Past few days the weather have been very cold. Alex was brought into Emergency Department with a low grade fever, rhinorrhea and poor feeding. On examination, he was found to be tachypnic and tachycardic. There was a soft systolic murmur. Few crepitation was heard over the lung field. Liver is palpable 3cm below the costal margin. An ECG was done as part of the work up for the murmur.

What is the most likely diagnosis.

A) Bronchiolitis

B) Tetralogy of Fallot

C) Anomalous origin of the left coronary artery arising from the pulmonary artery

D) Coarctation of the aorta

E) Ventricular Septal Defect

*

Reference:

http://www.emedicine.com/ped/TOPIC2484.HTM

*

Written by CH LEE on 9/9/2008

About my MCQ.

Please give suggestions and update to this question. Click on comments below for answer.

***

Related MCQ

Paeds ECG MCQ

]]> http://stglibrarynhs.wordpress.com/?p=32 Tue, 02 Sep 2008 10:58:17 +0000 nhslissgul http://stglibrarynhs.pl.wordpress.com/2008/09/02/medical-masterclass/ The Library has received a copy of the Royal College of Physicians Medical Masterclass, a study package aimed at doctors who are undertaking MRCP examinations (all parts).  Medical Masterclass comprises of twelve paper-based modules, two CD-ROMs and a website.

For more information, check out the Medical Masterclass FAQ's page at:

http://www.medical-masterclass.com/FAQ.aspx

Contact the library helpdesk for access to the website on 020 8725 0596 (int ext 0596).

Fortunately the pharmacist accepted the private prescription written on some lined note paper ripped out of a note pad - she'd told me that she'd dispense it if it was written on toilet paper as long as it was by a registered doctor she could find on the GMC's Online Register.  One injection of testosterone later I was still feeling exhausted - but I was considerably more interested in sex. So my exhaustion wasn't something easily fixable with testosterone.

Next step was too look for my suit and have it cleaned - seemed easy enough. Except after a through search of my bedroom floor I couldn't find it. It didn't seem to be in my wardrobe either. I found a jacket for which the trousers had worn out and spent a panicked half hour comparing the black trousers I had to the jacket to see which was close enough for a match.

Then I finally found the suit - in guess what - a suit carrier in my wardrobe - who would have though - if you know me that the last place I'm likely to find a suit is in a suit carrier. But by this time it was far too late to have it cleaned.

Fortunately it was quite clean so I hoped I could get away with it.

When I got the date for PACES I was surprised because it was on a Sunday - also because it was about 45 minutes drive from my girlfriends. As getting up at 7.15am on a Sunday wasn't her idea of fun we decided to book a hotel. Except you can't book a hotel without a credit card and when I asked her to book a hotel she baulked at the idea of spending £50 on a hotel 45 minutes drive from her house. So we decided to stay at hers.

I decided to practice ophthalmoscopy on her - and was struggling a little due to smudge on my opthalmoscope. She decided to clean it using some CD cleaning fluid and afterward I could barely see anything at all. Humm. Balls

Anyway.

We woke up in time and got to the hospital in plenty of time - half an hour before the report time. For such a big exam it seemed quite a causal affair. The sign to the PACES exam was hand written with a marker pen.. for instance. The exam was in a small day surgery unit in a small DGH, such a normal place - not a grand hall at all. The examiners were just consultants who were doing this in there spare time.

We waited around for an hour and ten minutes before we got started - we had to put our name and exam number on the 14 marking sheets which you carry around from station to station and give to the examiner.

We chatting at first - but as the time came near we got more nervous. I told myself I was going to fail anyway so there was nothing to be scared of.

So this is what happened...

Station 4 - 'Communication Skills and Ethics'

This was where I had to deal with an 'Actor' (actually a secretary) angry at the fact her father had been admitted 7 days ago and now had pressure sores and MRSA. It was a bit awkward, at one stage she asked me if the stroke ward had the same number of nurses as a normal ward - I replied that it did. Because it does at the hospital I worked at, and if the nurses had been turning him properly - at this stage I showed her an imaginary turn chart which proved they had been.

During the discussion the examiners asked me why I told that the staffing on the stroke ward was the same as ours - I said because it was at our hospital and I would check if I didn't know. And also why did I pretend to look at imaginary documents? I did point out that I didn't do that in real life.

Station 5 Bits and Bobs

The first patient threw me - she had some scars on her legs and was short. And they told me the diagnoses was related to endocrinology. Humm. I struggled a bit and eventually looked at her hands to see if she had a short 4th and 5th metatarsal. She didn't but the examiner seemed to like that so I mentioned rickets. I asked what the Calcium was (low) and phosphate (low). They asked me if I could measure Vitamin D Directly - and I couldn't remember if you could - they told me hers was high. I mentioned vitamin D resitant rickets and we moved on to the next patient.

They told me he had difficulty swallowing, he had obvious neurofibromas over his arms and he said he daughter had similar problems when I asked. So Neurofibromatosis - but what was the connection was swallowing problems? I couldn't work it out and blundered about a bit and said there was known to be a link. They asked how I'd manage him and make a diagnosis - again I couldn't remember.

Next patient was a man with lower back pain - the only abnormality I could find was a loss of flextion of the lumbar spine. I wondered if it could be early Ank Spond and talked about that. I couldn't remember any of the associations or how to manage it.

Now the only thing I did really well in any of the examination stations - ophthalmoscopy - the one thing I thought I wouldn't be good at. This was why I went on the Ealing Neuropaces course. It was obvious optic atropy in a patient in a wheelchair - I thought it could be related to MS. But couldn't remember the most up to date way to treat a flare up of MS.

Station 1 Respiratory and Abdominal

I examined the abdomen ok - but finished a little before the allocated time - so probably missed something. The examiner was a bit nasty - I got the impression I didn't do well. He asked why I thought dilated veins on the upper abdomen were relevant and where the normal anatomical marker of the upper border of the liver was. By this stage I was in too much of a state to actually think of anything but 'about there' and point to it. I finally managed to come out with the anatomical landmark

The respiratory station was a lady with a chest wall deformity who was recently complaining of fatigue.  I found the chest wall deformity easily enough - and presented the case ok. Though I couldn't think of the term kyphoscolosis - fuck knows why, nerves I think. I couldn't think why she might be fatigued recently. The examiner asked how I'd manage her - I answered including O2 Sats - he said 'night or day?' and I realised they were getting at her having OSA from her chest wall deformity - the bell went and I quickly mentioned the way I'd investigate it.

Station 2 History Taking

The one station that went really well. It was taking a history from a young girl who had had her first seizure - I did this pretty well, answered all her questions and counselled her on work and driving and stuff.

Station 3 Cardiovascular and Neuro

The cardio was difficult - the patient had a sternotomy scar and a loud second heart sound - I also thought that she had a disastolic murmur of AI. Except I wasn't confident enough to say this at first and was rather hesitant about presenting it. Stupidly I only mentioned measuring the BP when I talked about management - there was a really wide pulse pressure. If I'd asked earlier I'd have been more confident about staying there was AI.

Neuro - the sort of thing that gives me flashbacks. I examined the upper limbs of the lady - weakness of the elbows and right wrist and absent reflexes and muscle wasting. I thought 'is this facio-scapular-humeral dystropy' as I was examining - but when I came to present my findings I forgot about it. And to make it worse I just couldn't think of a diagnosis that fitting the findings - all the suggestions I could think of were 'well it could be a parasaggital mengioma but that would be different'.

As we left I worked out with the other candidates that it was probably 'limb girdle muscular dystopy'. Why didn't I notice this?

I don't think I passed. I don't think I deserve to have passed. In fact I really don't think I want to be a member of any Royal College that admits me after that performance.

A 5 years old boy with Atrial Septal Defect attended for pre-operative medical examination. He had a irregular pulse. Attached is the ECG of this child.

Click on ECG to enlarge the picture

1. What is the diagnosis?

A) Sinus arrhythmia

B) Wandering Atrial Pacemaker

C) Atrial Fibrilation

D) Complete Heart Block

E) Second Degree Heart Block

2. What is the significance of this finding?

A) no clinical significance

B) This child is at risk of sudden death from cardiac arrhythmias

C) This child is in cardiac failure

D) This child needs a permanent cardiac pacemaker implantation

E) This child needs anticoagulation

Written by CH LEE on 31/5/2008

About my MCQ.

Please give suggestions and update to this question. Click on comments below for answer.

***

Related MCQ

Paeds ECG MCQ 2

http://chenghiang.wordpress.com/2008/09/09/paeds-ecg-2/

Its just like when you've been driving a car for years, and you don't have to actively think about the pedals and shifting the gears. Of course this will only come with repeated practice.

I'll share my Thyroid package with readers, and hope it helps some to develop their own routine.

In PACES you are most likely to get a Hyperthyroid case, and be asked to examine the eyes, the neck or comment on thyroid status.

PROTOCOL

1) Quick general examination, and cursory look at the whole patient. Is he fidgety or anxious and sweaty? Is there obvious proptosis? Is there a goitre?

2) Examine the hands for fine tremor, palmar erythema and thyroid acropatchy.

3) Feel the pulse, specifically looking for Atrial fibrillation.

4) Work your way up and check for proximal myopathy by quickly checking power in shoulders and upper arm abduction against resistance.

5) Look at the neck. Palpate after asking patient to swallow with a glass of water, and feel for nodules etc.

6) Percuss for retrosternal goitre, and auscultate for a thyroid bruit

7)Move to the eyes. Look from the sides and from above to look for proptosis, and note any lid retraction. Check for lid lag, and check eye movements.

8) Examine the legs for pretibial myxedema, (and check ankle reflexes if have time)

9) Tell the examiners you would check BP, as these patients can have isolated systolic hypertension.

A mnemonic for Thyroid cancers, unlikely to be asked in PACES, but useful for MCQs (in order of decreasing frequency):

Papa Fought Against Mama.

Papillary, most common thyroid cancer, good prognosis

Follicular

Anaplastic

Medullary, associated with MEN syndromes.

The mnemonic is also good for remembering frequency of occurrence of the cancers with Papillary at the start being most common, and Medullary last being least common.

Personally I prefer Balligas' "250 Cases in clinical medicine", because it contains a lot of information that is useful for clinical practice beyond PACES (perhaps thats why he hasn't labeled it: 250 cases for MRCP!!) as well as little tid bits of historical information, and other clinical gems. His Q & A format is novel, and he is able to back up a lot of his answers with reference to medical literature.

Within the confines of PACES and strict time limits, examiners don't have the time to ask all the questions that Balliga poses, but he acknowledges that by labeling these questions "Advanced Questions". I also like the way he links the findings with possible aetiology and functional status (this is often overlooked by examinees.)

If time is short, and you want a book specifically to pass PACES then Ryder and Mir "An Aid to MRCP PACES"
is particularly useful. They list cases in order of frequency in exams recently sat , as well as giving good advice about exam techniques and salient features in disease. Volume 2 is useful if you practice history and ethics scenarios with a friend.

PACES for the MRCP by Tim Hall is good if you want something cheaper but glossy and attractive with diagrams and colour! It is also a very good book, written in a fairly straight forward and simple style.

I did buy "Neurology for PACES" by Pastest. This is a sheer waste of money. The above books are good enough. The book is bland and boring, and not particularly a good read.

You can check these books out in the link below:

Amazon.co.uk Widgets

1) Start early about 2-3 months before the exam date.

2) Design a timetable and establish a group of people going for the exams at the same time.

3) Buddy together and produce a rota with consultants on it willing to teach.

4) Locate interesting cases from e.g. acute take and grill each other. My group had a chart on the receiving unit attached to the white board. Everyone chipped in and put the names of patients to go and see, and which system to examine on it. It didn't have to be patients on the acute ward, it could be patients anywhere.

5) Be ruthless to each other, don't be softly, softly.

6) Practice presentation skills again and again, even with patients you see on acute take. Do it in your head or in front of the mirror.

7) keep a notepad of cases you see, and the salient features that you found. Practice presentation of these cases, and write on the pad, as you would, were you to present the case orally.

8) Be prepared to spend time after work to do all the above and see at least a different case a day.

9) Find out if your hospital/or a friends hospital does PACES and go down and see the cases before the exam, or even participate in helping run the exam. Will give you confidence and look good on your CV.

When I sat the exam, we had an excellent group, who kept each other informed about good cases, and paged each other if there was anything in clinic. I remember once being paged by a colleague to see the most grotesque gouty hands you could imagine, but it was good because you had to talk about it and remember to look at other joints and at the ears.

But you know doing it this way you won't miss any major (or even rarer) cases, and won't be fazed on the day of the exam.

DO I need to go on a course?

To be honest, NO.

I did go on a course, but I had a study budget and had to use the money or else I'd lose it, but if you stick to what I have said above that is more than enough.

Which course did you go on?

PACES ahead course at St Georges in London. Can't really recommend it. Some of these people who organise these courses treat the PACES candidates like milk cows.

They had way too many candidates for the weekend course, so obviously you can't see every case. A few of the consultants (esp a specific gastro guy) very extremely rude and didn't really care despite the fact we were paying them money to teach us! How sick is that! Got to say though very lucrative.

What should I wear?

Wear professional attire, just as you would for a job interview, i.e. suit, shirt and tie for males and modest suit or dress for ladies.

Finally make sure you know the location of the center, book accommodation or stay with a friend
the night before and rest fully because you will need to keep your wits about you for the day. Check all documents/ID before you leave for the exam.

1) Gastro: Hepatomegaly, discuss causes and Investigations

2) Resp: interstitial fibrosis, discussed differentials, causes

3) Neuro: paraplegia in guy with MS. Again examiners asked about differentials. Type of lesion i.e. LMN vs UMN.

4) Cardio: classic Aortic Stenosis, with slow rising pulse, ESM to carotids, asked how you would treat and when aortic valve should be replaced.

Don't forget in AS you DON'T want to reduce the afterload, as can cause sudden death esp in severe AS. Therefore, avoid nitrates and ACE-i, and use Beta blockers instead.

In Aortic regurgitation (AR), you WANT to reduce Afterload. Remember it this way: AR is Afterload Reduction. So give ACE-i, or hydralazine.

5)short cases: Diabetic retinopathy with photocoagulation scars, psoriasis, rheumatoid hands, treated thyrotoxicosis.

6) ethics: women who is pregnant has had PTE, discuss the diagnosis with the patient and tell her treatment options.

7)History taking: women c/o increasing SOB, on OCP, had syncopal episode. Examiners asked about diagnosis, tests, sounded like chronic pulmonary hypertension possibly secondary to chronic pulmonary emboli.

Thought my exam was fair nothing exotic, although I've heard stories of other experiences which aren't so nice. I've helped arrange 2 MRCP PACES exams, and if there are any weird cases floating around they usually are called.

Don't forget polio, pseudoxanthoma elasticum (plucked chicken appearance to skin), muscular (incl scapular variant) dystrophy, myotonic dystrophy and retinitis pigmentosum! They love these cases.

Pseudoxanthoma elasticum:

www.dermatlas.org/derm/result.cfm?Diagnosis=-1870527506

Retinitis pigmentosa:

www.dermatlas.org/derm/result.cfm?Author=1024406765

Common mistakes:

1)confusing photocoagulation scars in diabetic eyes with retinitis pigmentosa (RP). Remember RP affects both eyes on the periphery with spiculated appearance. There may be other signs of diabetes e.g. exudates, heamorrhages. Look at fingers for evidence of finger pricks in DM from glucose monitoring.

2) Rheumatoid hands vs. psoariatic arthropathy. Look at skin, check for rheumatoid nodules at elbows. If distal IP joints affected unlikely to be Rheumatoid.

3) Failing to check for clonus and assessing gait in the neurological examination

4) Not appreciating the difference between lower and upper motor neuron signs. You would think that is basic, but in an exam situation it is easy to get messed up.

Just to remind you...

Lower motor neuron lesion: The lesion is anywhere from the ventral horn cell body to the muscle synapse. There is wasting, fasiculation, and areflexia.

Upper motor neuron lesion: Anywhere from above the cell body to the brain.

There is spasticity, hyperreflexia, and clonus. There may be a so called 'scissor gait'. Wasting is not usually so profound.

5) In the abdo exam make sure you palpate sitting on a chair or kneeling on the floor. The patient should be lying on one cushion or as flat as possible, without discomfort (always ask). In my exam the patients' bed had been jacked up really high. I lowered the bed, and sat on a chair to palpate. They do these tricks to check your exam etiquette. Don't forget to auscultate.

6) A lot of candidates get flustered when they have a resp case where the patient has had a previous lobectomy. know the indications e.g. resection of bronchial ca, TB (was an old treatment pre antibiotics), bronchiectasis.

7) Forgetting to mention you would check BP in the Cardiovascular case.

Finally, the grilling after the cases weren't that difficult, my medical school end of block clinicals were more intense. To be fair however, time limits weren't as strictly adhered to as in PACES!!

It is composed of 3 stages, Part 1 and Part 2 Best Of Five MCQs and a clinical examination with several stations called PACES (Practical Assessment of Clinical Examination Skills).

There is much debate about this, but I personally feel it is not that robust an exam, certainly the USMLE is generally far more rigorous, and thats an undergraduate examination! Perhaps this is one reason why Knowledge based assessment exams have been created before one can complete specialty training?

Although we'll have to wait to see the standard of these assessments, and whether or not they are up to scratch, before candidates take up sub consultancy (emphasis added).

I would certainly not recommend any foreign doctors to waste their time and money taking the test, unless they want some letters after their name, because their is a crisis in British medicine with many home grown doctors expected not to have jobs in the coming years, let alone foreigners who want to enter the system.

Anyhow if people are really keen here are my tips:

MRCP part 1: I scored 77%, with the pass mark at 62%.

Largely short clinical vignettes, with some basic science questions.

I would use only Philip Karla "Essential revision notes for MRCP", and Onexamination.com online questions
. Don't waste money on courses (unless you have an allocated study budget!)

Onexamination is interesting, prob about 5% of questions are verbatim word for word similar to questions on the exam, which is a bit fishy, because that is illegal, but I suspect they are probably linked in some way to the Colleges and can get away with it.

Caution: Please don't waste money on the Masterclass series by the colleges. My hospital had free access to it from the library, and the questions were not typical of the exam. I found the overall software very poor, and the questions absolutely rubbish. I think access to the program and books etc is about £500 in total, so it ain't cheap.

MRCP part 2: I scored 72%, with pass mark at 57%.

Harder exam, with longer vignettes, and a lot of so called grey cases.

Again Onexamination quite good for this, a revision course may be useful, but just practice lots of MCQs.

Both these exams have criterion referenced pass marks which are pretty achievable usually 55-60% is all that is needed. Whether a person passes by 1 mark or 20 marks, this is not considered in selection or progression for higher training at the current time.

PACES: Again very doable, but more nerve racking as you are being objectively assessed, usually 5 stations, including a history taking station and a separate station for ethics/communication.

Practice, practice, practice on the wards, find those interesting cases, and work with others taking the exam to improve skills, Balligas' 250 cases for the MRCP is a really good book, but goes into greater depth than is really needed for the MRCP nowdays.

More information:

1) Official Colleges MRCP website:

www.mrcpuk.org/

2) study on MRCP examination standards:

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1185541

Forget what it stands for PACES is scary, PACES is torture. PACES is an exam that involves examining patients with clinical signs whilst being watched by a scary professor type, then they quiz you on how you made your diagnosis. I've known Doctors who were doing PACES since Medschool, and they seemed godlike types with amazing clinical skills. I can't do PACES, I can't be that good.

I remember when I was a third year and had just landed in hospitals, and just couldn't understand how doctors could get as excited as they did over a heart murmur of all things. I couldn't understand this until last week when I detected a Tricuspid Regurg, do you know how rare Tricuspid Regurg is?

The thing is that really, in real life we often manage to make diagnosis without having to examine patients clinically - take neurology - in the old days diagnosis used to involve a pinwheel, red and white hatpins and a tendon hammer, now we mainly just use a tendon hammer. It's easy to cut corners, and it's easy to rely on your test results a bit too much. So is it a cellulits or a DVT? easy if you can do some blood tests and a scan. Difficult if you just have to look at them.

So we had PACES practice today and actually I wasn't bad at all, I'm not over confident by any means, but got the hint that if I work really really really hard it means I might actually pass.

Which of the following test is the best indicator for active viral replication in Hepatitis-B?

A. Hepatitis B Surface Antigen

B. Hepatitis B Surface Antibody

C. Total Hepatitis B core Antibody

D. Hepatitis B e Antigen

E. Hepatitis B e Antibody

Similar question in FRACP (paeds) 2008

Written by CH LEE on 13/3/2008

About my MCQ.

Please give suggestions and update to this question. Click on comments below for answer.

Mechanism of action of Infliximab in Crohn's Disease

A) Bind to TNF alpha

B) Block TNF alpha receptor

C) Reduce TNF alpha production

D) Reduce TNF alpha secretion

E) Increase hepatic metabolism of TNF alpha

Similar question in FRACP (paeds) 2008

Written by CH LEE on7/3/2008

About my MCQ.

Please give suggestions and update to this question. Click on comments below for answer.

Life has been nice. What's been going on? Well...

I got back 2 days ago from a 5 day mountaineering course up in Scotland with my friend Becka. It was AWESOME! Ha. Flew up to Inverness and then caught the train to Aviemore / Cairngorm National Park. I am now the (very) proud owner of an ice axe and crampons, not to mention rather a lot of expensive clothing: I own 'technical trousers' (even after wearing them for a week I'm not entirely sure what 'technical trousers' are though I did manage to put 3 holes in them with my axe). So yeah, climbing and generally arsing around in snow. The strangest thing: while half way up Jacob's Ladder, barely able to see because my glasses were frozen and a mass of spin drift was tearing past us from below, the main thoughts going through my head were not 'Fucking hell it's freezing', or 'what am I doing here?' but 'This is simply amazing. I love this'. Yeah, turns out that along with walking I really like winter mountaineering. Shame I live so far away from mountains...

I passed MRCP part 1 (first professional/post-grad exam) which was a genuine surprise. I mean I worked fairly hard but didn't feel that confident and I'm usually pretty good at knowing how well I did after the exam. But I passed. Which is nice. However, now I'm wondering about sitting part 2. I mean I don't need to sit these exams as I want to be a GP and I only sat part 1 to kickstart my revision and further learning (which has worked) but it would be nice to keep at it and build on the knowledge. The timing doesn't work though as I can only sit it in July (too soon) or December (not in the country) and even then, if I passed I'd have to sit PACES within 2 years and I can't guarantee that as I may not be back by then. Still.

So I won't be in the country as I'm moving to New Zealand for the next 2 years. That's the plan anyway. Annoyingly I can't apply for a job until May as I can't start until November which is rather worrying, especially with the job crisis here. However, I've got a pretty good CV now and it should all be fine. Katherine (my missus) has a job already in Christchurch which is where I'm intending to go too. Lots of reasons why I want to leave here. Maybe another time.

The reason I can't start till November is I'm headed back to Nepal as part of a medical research expedition to the Hidden Valley behind Dhaulagiri - I'm acting both as a medical officer and research coordinator. Which should be cool. A 5 week trek to camp at 5100m for a week, studying various effects of high altitude.

So yeah, lots of stuff and much more besides. Plus the Los Campesinos! album has finally come out - and it is glorious.

For now though...

Diencephalic Syndrome

A) common cause of failure to thrive in infant

B) associated with absence of subcutaneous fat

C) hyperkinesia and hyperalertness are observed in children with Diencephalic Syndrome

D) affected children have significant reduced caloric intake

E) associated with brain tumour.

Written by CH LEE on 29/2/2008

About my MCQ.

Please give suggestions and update to this question. Click on comments below for answer.

Kiedyś odbywało to się w ten sposób, że należało zadzwonić do BOK i cierpliwie czekać, aż ktoś "z tamtej strony" odbierze nasz telefon. Następnie przychodził czas na autoryzację, czyli podawanie numeru PESEL, seria i nr dowodu osobistego oraz nazwisko panieńskie matki. Dopiero po tych zmaganiach Konsultant czytał przez telefon kwotę salda widniejącą w systemie. Nie wiem czy jeszcze są banki, które jeszcze tak robią, miejmy nadziej, że nie.

Spotkałem się również z rozwiązaniem opartym na nagraniach lektorskich. Polega to na tym, że tworzymy nagrania, w których lektor czyta ciągi cyfr. Następnie ta baza plików audio są dzielone na małe fragmenty i sklejane przy odczytywaniu salda konta, np. kwotę 1234 taki system przeczyta nam jako 4 osobne cyfry - 'tysiąc' 'dwieście' 'trzydzieści' 'cztery'. Niestety to daje bardzo mizerny efekt.

Czas na syntezator mowy opisany na początku- jakie daje możliwości w stosunku do powyższego? Na pewno jest rozwiązaniem jakościowo znacznie lepszym, o czym możecie się przekonać na stronie say.expressivo.com gdzie można przetestować tą technologię na dowolnym tekście.

Warto również dodać, że text-to-speech (TTS) daje ogromną elastyczność, ponieważ program ten przeczyta dowolny tekst, naprawdę dowolny! Dla testów wpisz na powyższej stronie słowo "kasztypki"lub "na koncie masz 1200356 złotych" ;)

Jakie są inne korzyści? Najważniejszą korzyścią dla firm wykorzystujących tą technologie w biurach obsługi klienta to odciążenie agentów siedzących w CallCenter, ponieważ gro ich obowiązków przejmuje właśnie zautomatyzowany system obsługi klienta korzystający z TTS. Oprócz salda konta można wykorzystać tą technologię do czytania ostatnich operacji na koncie (daty, odbiorcy) czy też odczytać informację o wszczęciu postępowania egzekucyjnego. Możliwości jest od groma, a ide jedna - zaoszczędzony czas agentów przeznaczyć na inne czynności.

Od strony technicznej wygląda to w następujący sposób. Potrzebujemy platformę IVR (Interactive Voice Response), która jest podłączona do różnych baz danych w banku. Następnie integrujemy z IVRem na przykład syntezator mowy IVONA Telecom i dzięki temu w telefonicznym biurze obsługi klient możemy odczytać przez telefon... tak naprawdę wszystko.

Dodam jeszcze, że taki system jest niesamowicie skalowalny dzięki zastosowaniu protokołu MRCP, ale o tym innym razem.

Alopecia in children, what is the most likely diagnosis in the following clinical scenario.

1. Tracey is a 8 years old girl. Her mother brought her to see you for new onset hair lost. She is otherwise healthy and previously had normal hair. The family is going through a difficult time, as her parents are separating. There is a small patch of hair loss, she did not complaint of itchiness or pain. On examination, the skin in the area was smooth and normal looking; there were no erythema or flaking. On closer examination, there were a few “exclamation-point” hair. Wood's lamp examination revealed no area of fluorescence. There was no cervical lymphadenopathy. There were nails pitting and grooving of the nail plate.

2. Gina is a 8 years old girl. Her mother brought her to see you for new onset hair lost. She is otherwise healthy and previously had normal hair. The family is going through a difficult time, as her parents are separating. There is a small patch of hair loss, she did not complaint of itchiness or pain. On examination, the skin in the area is normal looking; there were no erythema or flaking. On closer examination, there were short and medium length, stubbly hair. There were no “exclamation point” hair, all hair were of full thickness and did not taper. Wood's lamp examination revealed no area of fluorescence. There was no cervical lymphadenopathy. Her nails had irregular edges.

3. Amy is a 8 years old girl. Her mother brought her to see you for new onset hair lost. She is otherwise healthy and previously had normal hair. The family is going through a difficult time, as her parents are separating. There is a small patch of hair loss, it is itchy but not painful. On examination, there was scaling and erythema of the affected area. On closer examination, there were small pustules on the scalp. Wood's lamp examination reveals an area of fluorescence. There was cervical lymphadenopathy. She was chewing on her nails while being examined.

4. Amy is a 8 years old girl. Her mother brought her to see you for new onset hair lost. She is otherwise healthy and previously had normal hair. The family is going through a difficult time, as her parents are separating. There is a small patch of hair loss, it is not itchy or painful. She complaint that her hair is falling out in clumps. On examination, the skin in the area is normal looking. There was no “exclamation-point hair”. Hair pull test is positive. Wood's lamp examination revealed no area of fluorescence. There was no cervical lymphadenopathy. She was chewing on her nails while being examined.

A. Tinea Capitis

B. Telogen effluvium

C. Androgenetic Alopecia

D. Alopecia Areata

E. male-pattern baldness

F. Trichotillomania

G. Scarring Alopecia

 Reference:  Arch. Dis. Child. Ed. Pract. 2007; 92: 193-198. doi:10.1136/adc.2007.130781

Written by CH LEE on 23/1/2008

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This is generally good - however the bad thing is that Clare and I are of the chosen ones, who will be employed for the next 8 years as long as we pass appropriate exams. John on the other hand is an FTSTA - he has to get back into the system when one of the chosen ones drops out. Clare and I got this because we might have done slightly better in some stupid assessment centre than he did - he's not a worse doctor than us by a long stretch of the imagination. He's certainly better than me.

Anyway - we studied together, I went on a course with John, Clare went on a different course. We studied past papers on the floor of the flat I was renting, endlessly, we obsessed together. We were convinced we'd fail together. John, had already failed before and was fairly convinced he would do again.
We didn't sit the exam at the same place - but after the exam we exchanged endless text messages together comparing our answers to the questions. We were all convinced we'd fail together.

The exam results were due out of the 7th, we were pscyhed up for the 7th, I planned to go away for the weekend with The Wonderful Girlfriend, to take my mind off it.

On Thursday John noticed our exam status has changed from 'Application accepted' to 'result pending' which last time meant the results were out the next day. As we were walking to work I noticed two magpies which I took to be a good omen.I obviously know this really means nothing,

Friday was busy - but I was on my own in the morning - so I checked the MRCP website nearly every hour, when they hadn't published them by lunchtime I decided they probably weren't going to be out that day. Clare and I agreed that the first one to find out that the results were out would page the other one.

At 4pm, when I was checking the my routine blood results on the Ward Computer - when I thought that I'd just quickly check my the website. And there it was. The screen said 'Results Released' - but I couldn't see the results. I scrolled down the screen. And there it was. 'Pass'.

Pass? I can't have passed.

I told my Registrar, who was the nearest person, who said 'Congratulations - now can you get on with your job'.

But I needed to know how Clare and John did, we'd spent so much time revising together. I really wanted John to pass, because he was so close to loosing hope if it didn't. I wanted Clare to pass as well. But most of all I wanted me to pass.

I bleeped Clare first - there was an awkward moment, when we didn't want to ask the other one what happened. But she'd passed as well.

About ten minutes later John popped into my ward - I was assisting my Reg with a sterile procedure. He mouthed 'what happened' from the other side of the ward. I gave a thumbs up sign - and he smiled and said 'me too'.

This was unbelievable - we'd all passed. This means we'll be doing PACES together as well.

But the kick in the teeth is that whilst Clare and I have a job for 8 years (as long as we pass exams, and we're ahead of time already). But John doesn't - John has to re apply for a job next and there are hardly any of them. Even with the exams.

1. The most common cause of nephrotic syndrome in paediatrics population is

A) Minimal change disease

B) Mesangial proliferation

C) Focal segmental glomerulosclerosis

D) Membranous nephropathy

E) membranoproliferative glomerulonephritis

2. Below are the characteristic features of nephrotic syndrome EXCEPT

A) Proteinuria more than 40mg/m²/hour

B) Hypoalbuminaemia

C) gross haematuria

D) Oedema

E) Hyperlipidaemia

True/false questions.

3. In Minimal change disease

A) gromeruli appear normal on light microscopy

B) Immunofluorescence microscopy show IgM and C3 staining.

C) Most children will response to corticosteroids treatment

D) Renal biopsy is indicated to confirm diagnosis before starting treatment

E) Most children will have end stage renal failure

4. Features that make minimal change disease less likely includes

A) Less than 1 year old at presentation

B) Hematuria

C) Hypertension

D) Renal insufficiency

E) Hypocomplementemia

5. Focal segmented glomerulosclerosis

A) Account for 10% of children with idiopathic nephrotic syndrome

B) Immunofluorescence microscopy show IgM and C3 staining.

C) Most children will response to corticosteroids treatment.

D) Most children will have end stage renal failure.

E) Light microscopy show mesangial proliferation and segmental scaring.

6. Management of idiopathic nephrotic syndrome

A) Low sodium diet play a role

B) Fluid restriction may be necessary

C) Diuretic use is associated with decrease risk of thromboembolic complication

D) with presumed minimal change disease, prednisone is administered for 5 days.

E) cyclophosphamide can be used in patient with steroid resistant disease.

Written by CH LEE on 5/1/2008

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Wilms Tumour is associated with the following syndromes except

A) WAGR syndrome

B) Denys-Drash Syndrome

C) Beckwith-Wiedemann Syndrome

D) Down's Syndrome

E) Perlman Syndrome

Written by CH LEE on 31/12/2007

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Dancing eyes and dancing feet syndrome (opsomyoclonus) is most commonly associated with,

A) Neuroblastoma.

B) Variant Creutzfeldt-Jakob disease

C) Parkinson disease

D) Medulloblastoma

E) Multiple Sclerosis

Written by CH LEE on 31/12/2007

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Children with Down Syndrome

A) acute leukemia is less common than general population

B) AML is more common than ALL

C) prognosis in AML is better than general population

D) diagnosed with ALL should be given a higher dose of methotrexate

E) Neonates with Down syndrome who developed myeloproliferative syndrome, need to have immediate high dose chemotherapy.

Written by CH LEE on 31/12/2007

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Red Man Syndrome.

A. Is commonly seen after second oral dose of penicillin

B. Is a anaphylactic reaction

C. Is cause by mast cells degranulation

D. Also called “red bottom syndrome” in paediatrics, as the erythematous rash in children with red man syndrome is seen mainly around the gluteal region.

E. Must be treated immediately with IM adrenaline.

Written by CH LEE on 16/12/2007

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