PACES MRCP UK - Where MRCPians Meet Since 2006

Frank's sign

2008-08-27T18:47:00.002+08:00

Spotted this recent post by Wuchereria in his new blog. I learnt a new sign - Frank's sign. He highlighted that this is a great sign to impress the examiner!

"I just got back from Hong Kong recently for a holiday.During a morning of breakfast, while I looked around I noticed this man who was sitting eating 'Tim Sum' and I am sure he has coronary artery disease.
There was obvious Frank's sign.

Frank's sign is a diagonal crease in the lobule of the auricle :
Grade 3 - a deep cleft across the whole earlobe
Grade 2a - crease more than halfway across the lobe
Grade 2b - crease across the lobe, but superficial
Grade 1 - lesser degree of wrinkling

Ear lobe creases are associated statistically with coronary artery disease in most of the population groups."

Optic atrophy

2008-07-30T15:05:00.003+08:00

Look for:

in young patient, mention you like to examine the eyes for internuclear ophthalmoplegia and cerebellar sign for multiple sclerosis
Signs of Cushing's syndrome in SLE pts on steroid
in old patient, look for evidence of vascular diseases such as prominent temporal artery (or old scar indicating temporal artery biopsy) and carotid bruit

(or endarterectomy scar)

Congenital

If congenital, it is usually hereditary with an onset of deterioration in childhood and may be accompanied by nystagmus. Leber's Hereditary Optic Neuropathy, (LHON) or Leber Optic Atrophy is hereditary, but typically has its onset in 20-30 year old males. This is due to a mutation of the mitochondrial genome and hence is passed exclusively through the mothers. Dominant optic atrophy or Kjer's optic neuropathy has autosomal dominant inheritance. It usually presents in early childhood. There are numerous less common genetically related syndromes.^[2]

Alternatively, congenital optic atrophy can be caused by a lack of oxygen during pregnancy, labour or in the early days of a child's life. Some drugs taken during pregnancy are also associated with optic atrophy.

Acquired

The acquired type of optic atrophy may be due to blood supply changes in the eye or optic nerve (anterior ischemic optic neuropathy or posterior ischemic optic neuropathy), may be secondary to inflammation or swelling within the optic nerve (optic neuritis), may be a result of pressure against the optic nerve (such as from a tumour), or may be related to metabolic diseases (e.g., diabetes mellitus), trauma, glaucoma, or toxicity (caused by methanol, tobacco, or other poisons). It is also seen in vitamin B12 deficiency and Paget's disease of the bone.

Googling to save lives?

2008-07-26T23:14:00.002+08:00

In a clinical case discussion published on New England Journal of Medicine (July 3, 2008), medical experts opined that "Internet search engines, such as Google, are proving to be an invaluable diagnostic tool", given the rapidly growing body of medical knowledge.

An internet-based study revealed that Google searches may arrive at the correct diagnosis in ~58% of cases. Will this mean physicians may no longer be needed in the future?

Also available at http://tangwengheng.blogspot.com/2008/07/googling-to-save-lives.html

2nd MRCP PACES Preparatory Course

2008-07-15T23:04:00.006+08:00

The 2nd MRCP PACES Preparatory Course is finally in place. The organiser, wuchereria would like to take this opportunity to welcome participation from all.

Click here to download the course brochure (great design by wuchereria :) & the registration form.

The link will also be mirrored here.

If sending by mail, please address it to:

C/O Professor Richard Loh/ Dr TT Lim
2nd MRCP PACES Preparatory Course
Penang Medical College
No 4 Sepoy Lines,
10450 Penang
Malaysia

Upcoming 2nd MRCP PACES Preparatory Course

2008-06-02T09:53:00.006+08:00

I am pleased to say that recently there has been ample of emails and personal calling-ins to enquire for the 2nd MRCP PACES preparatory course.

The 1st MRCP PACES Preparatory Course which was held September last year had been a really fruitful one, with candidates passing rate of approaching 60%! Our heart-felt thanks to all the great teachers in our midst.

Unfortunately, I'd most probably be away in the next few months, hence wouldn't be able to host this course again this year. Our associate author, Wuchereria, will tentatively be planning for one.

We'll keep you all informed about the progress. Thanks again for the support!

Regards,
Axonopathic

PS: The comic is just a joke to cheer you all up :)

Cranial Nerves Examination Series II

2008-05-28T03:51:00.003+08:00

Cranial Nerves V and VII

Cranial Nerve VIIl

Cranial Nerves IX, X, XI, and XII

Cranial Nerves Examination Series I

2008-04-19T07:38:00.011+08:00

Hey, folks. It had been a long time from the last neurology post. I found some useful videos from Youtube. Hopefully, these video demonstrations will save you from having sympathetic overactivation in the neurology station!

Cranial Nerves I and II

Cranial Nerves III, IV and VI

To be continue..

Basic Echocardiography Workshop

2008-04-08T10:36:00.004+08:00

Basic Echocardiography Skills Training Workshop

Jointly Organised by,

Ministry of Health Malaysia

Cardiology Department, Penang Hospital & Penang Hospital Cardiology Society

Also In collaboration with,

Society of Cardiac Imaging Malaysia (SCIM)

Announcing Basic Echocardiography Skill Training Workshop which will be held on 25th-28th April 2008 in Penang Hospital, Malaysia.

This would be the first Echo course to be held in the northern region over the recent years. The organisers warmly welcome participation from all fellow colleagues who are interested in basic echocardiography.

Please click here to download the programme brochure.

Some Drills On Station 5 (Part 5)

2008-03-21T01:14:00.007+08:00

Station stem:
This patient presents with intensely itchy skin lesions on both lower limbs for a short duration. Please examine and lay down your differential diagnoses. What are the questions would you like to ask?

Above picture on the shin, and the following picture is on the anteromedial aspect of another leg:

And a close-up:

Happy Chinese New Year

2008-02-06T22:08:00.000+08:00

Dear all friends & MRCPians:

We would like to take this opportunity to wish all Chinese readers a happy, healthy and prosperous new year.

Wishing you & family "A Happy & Prosperous Chinese New Year 2008"

Quiz: Skin station

2008-02-04T09:30:00.000+08:00

This gentleman has multiple similar lesions distributed over face, limbs as well as trunk. Please describe the lesions.

What is the significance of these lesions?
Hint: related to any syndrome?

Quiz time again!

2008-01-31T06:29:00.001+08:00

You see this patient in Station 5: skin.

Describe the skin finding. Then, outline the other system involvements that are relevant to this condition.

Gynaecomastia in PACES

2008-01-25T08:58:00.001+08:00

This is a man !

The most important tool in PACES is Inspection.

However to differentiate a pass from a fail involves preparing for the exam and of course luck which is difficult to change except by praying hard for the exam. For the former, pls remember that the time for the cases are short and most that comes out from our mouth has been prepared before the exam

So, if you see this picture, always remember which station you are

Nobody will miss the gynaecomastia in the above man

Station 1 : Abdomen - Cirrhosis of liver

Station 1 - Resiratory - Bronchogenic carcinoma

Station 3 : Cardiovascular - Drugs (spironolactone/digoxin)

Station 3 : Neurology - Myotonic dystrophy

Station 5 : Endocrine - Klinefelter's syndrome

I know there are other causes of gynaecomastia such as adrenal... but my mentor (eMRCPian) once told me, always think PACES way when you are going for a PACES exam !!

So, the above patient has gynaecomastia from Klinefelter's syndrome, look for other signs of Klinefelter.

Written by Wuchereria

A Blessed Christmas & Joyful New Year Ahead!

2007-12-15T13:03:00.000+08:00

We from the PACESMRCPUK blog team would like to wish every fellow MRCPians and aspiring MRCPians a very fine holiday season to come:)

We'll kick start another 'season' after this. Stay tuned:)

Notes Of Congratulations!

2007-12-04T02:15:00.000+08:00

Congratulations to all my colleagues who have succeeded in the recent PACES diet!

Special congrats note for Wuchereria and Panhypopit who have been writing in this blog and finally succeeded in their quest!

Also a warm congratulation note for all my colleagues who had joined our "1st MRCP PACES Preparatory Course and Mock exam" and succeeded in their exam. Your success really inspired us further :)

May your journey as an MRCPian thrive further in years to come :)

Quiz: Skin Station

2007-10-29T05:57:00.000+08:00

Examine this 80 year old lady's hands and comment

(Hint, she should have died long ago, and yet's she's fit as a fiddle. Her mother had the same condition and died her 80s)

Cases and photos contributed by Giant Eagles

Course/ Mock Exam Cases Drill (Part 2)

2007-10-20T11:13:00.000+08:00

Verbal feedback from the the cardiovascular lecturers indicates that on the average, the candidates performance was quite satisfactory. Nonetheless, some cases were done poorly. I had to admit that some of the cardio cases in the course were considered rare, nonethess, I could bet to my bottom dollars that the registrar in-charge wouldn't hesitate to put them up for PACES if only they're readily available!

As I'd told a few of the candidates, rare cases tend to have a set of signs which is so classical that most examiners are fond of asking:)

And yes, I always believe that rare conditions rely heavily on us (physicians) to diagnose. After all, that's our duty as physicians right? Hence, we should be well prepared for that.

After finished examining the patient, gather your thoughts and face the music!

In summary, this gentleman has ample of signs to suggest the diagnosis of hypertrophic obstructive cardiomyopathy (HOCM). This is because he has a jerky peripheral pulse with a bifid carotid pulse. The apex beat has double impulses and it's not displaced. There is a grade 3 ejection systolic murmur best heard along the left lower sternal border which well accentuated by asking the patient to perform Valsalva maneuvers. There is no S3 or S4 gallop and there is no other signs to suggest cardiac failure.

I would ask for your permission to perform other dynamic maneuvers which would further support my diagnosis.

Examiner:"What dynamic maneuvers that you have in mind?"

I would ask this patient to change from standing stance to squatting position during my auscultation, paying particular attention to the intensity of the murmur. I would expect the murmur to be softer when he is in squatting position, and louder again when he's standing.

Examiner:"How would you investigate him?"

I would do a resting ECG first. I expect voltage-criteria left ventricular hyperthrophy to be evident on the ECG. There might be some secondary ST and T waves changes as well. I would reckon that a CXR in this most probably would be normal since during my examination, the apex beat is not displaced and hence I wouldn't expect cardiomegaly.

But really, an echocardiogram would clinch the diagnosis. Classical signs from echocardiogram would include asymmetrical septal hypertrophy (ASH) and systolic anterior motion (SAM) of the mitral valve.

Station 5: Fundus

2007-10-14T02:03:00.000+08:00

What is the diagnosis?

What else to look for?

Course/ Mock Exam Cases Drill

2007-10-12T18:13:00.000+08:00

Here are some of the cases for the preparatory course/ mock exam.

Case 1: Please examine this lady's hand and tell me your findings.

Case 2: This patient has difficulty in holding objects in her hands. Please examine her.

1st Preparatory Course And Mock Exam Experience

2007-10-05T18:57:00.000+08:00

The very 1st MRCP PACES preparatory course and mock exam has ended successfully in Penang Hospital. I wish to thank all my team mates and the participants for their support. I'm indeed grateful for being granted the task of putting up a great team for the event.

By saying a great team, I really mean it! We hope to make it an annual event:)

I would like to thank the following prominent academic gurus for their time and effort in teaching the candidates:
Prof Richard Loh
Prof Amir S Khir
Dato Dr Rozina
Dato Dr Abd Razak Muttalib
Prof Dato Kew
Prof Abd Rashid Abd Rahman
Prof Raymond Azman Ali
Dr Haniffah Abd Ghafoor
Dr Norazizah Aziz
A/Prof Malik Mumtaz
Dr Simon Lo
Dr Eow GB

Without their selfless contribution, this event would not possibly be realised!

PS: Special thanks to eMRCPian for his advice and moral support

Travelling Circus

2007-10-04T22:05:00.000+08:00

As correctly mentioned by one of the examiners, we are the travelling circus.......Travel from one hospital to another doing MRCP courses and Mock exams !
Taiping - Sungai Petani - Penang - Alor Setar (today)
Pheww......it has been tiring
? Tomorrow in KL
This is a tiring exam...just need to keep up till the big day.
Wishing all the best to all taking this time ! Don't worry if you don't make it. The circus goes on 3 times a year !
Anyone would like to share their experience for these few weeks of the circus ?

Quiz: Station 5

2007-10-02T13:20:00.000+08:00

Please look at this mentally challenged young man's hand and feet and proceed.

Case and pictures contributed by Giant Eagle

Station 5

2007-09-27T16:24:00.001+08:00

What is the diagnosis ?

This patient has epistaxis. What is it due to ?

Let's Stick To Our Basic!

2007-09-27T05:11:00.002+08:00

Spotted the post of palmdoc in MMR regarding Eternal Clerking. I absolutely agree with palmdoc. I still remember my professor in UM once said, an in-depth clearking and detail examinations are able to make >95% of the clinical diagnosis. We only need investigations to confirm the provisional diagnosis.

Undoubtedly, the advancement of modern medical diagnostic tools have changed the way of our practice. Sometimes, we are over dependent on these new gadgets until we forget the basic skills that we learned during our undergraduate days. In addition, defensive medical practitioner also rely on investigations to self-proof from medical legal issues.

All MRCPians, let's not to forget our eternal basic! I am sure we all can make an accurate clinical diagnosis in 13 minutes of detail history clerking and 5 mins of system examination.

All the best for your coming PACES in Oct/November!

Here is a great melody kudos on the essentials of clinical skills. Cheers!

Station 5

2007-09-26T20:30:00.000+08:00

What is the diagnosis ?

A Tale of Scar. Again?!

2007-09-26T20:24:00.001+08:00

My friend got this in his exam recently in London.

He was asked : what are the likely cause of this scar ?

Station 3 Cardio

2007-09-26T20:15:00.001+08:00

What is the sign shown ?
What is the diagnosis ?
What is the possible underlying valve lesion ?

Station 5

2007-09-25T20:37:00.000+08:00

What is the diagnosis ?
Any comments on this case ?

What'd Be Your Unifying Diagnosis?

2007-09-24T11:02:00.000+08:00

It's been a while since our last 'casual' life blogs.

I saw this lady during my combined antenatal and medical follow-up.

She had a congenital cardiac lesion which is corrected. Clinically she is pink on air and there is no finger clubbing.

What would you expect the lesion to be and what would be your diagnosis?

Quiz Station 5 Locomotor

2007-08-29T22:04:00.000+08:00

What is the diagnosis ?
How would you proceed to examine this patient ?
What is the cause ?

Quiz Fundus

2007-08-28T20:51:00.000+08:00

What is the diagnosis ?
What are the causes ?
How to treat ?

Station 5 Quiz

2007-08-12T16:01:00.000+08:00

What is the diagnosis ?

Some Drills On Station 5 (Part 5)

2007-08-10T15:17:00.000+08:00

Common and readily available case for PACES. Look at this patient's extremities and proceed.

What are your findings? What are the possible differential diagnoses?

How Would You Proceed?

2007-08-09T19:53:00.000+08:00

Spotted this patient while doing ward round. What is the clinical sign?

How would you proceed to examine him?

Photo contributed by Wuchereria

1st MRCP PACES Course And Mock Exam

2007-08-04T12:07:00.000+08:00

My dear fellow MRCPians, colleagues and friends,

I'm happy to announce that, after months of planning and head-cracking sessions with my colleagues in Penang Hospital and Penang Medical College, we've finally come up with the master plan of organising the very 1st MRCP PACES Preparatory Course and Mock exam on the 29th and 30th September 2007.

This event is envisioned from a joint effort between MOH Penang Hospital, SJ Hospital in collaboration with Penang Medical College.

This course and mock exam aims to prepare the local as well as outstation candidates for the coming Oct/Nov PACES diet.

We'll strive the best to help our fellow colleauges to get through this exam.

The course details and registration form is downloadable from here.

If sending by mail, please address it to:

C/O Professor Richard Loh/ Dr SK Ma
MRCP PACES Preparatory Course
Penang Medical College
No 4 Sepoy Lines,
10450 Penang
Malaysia

Cheers,

Axonopathic

Quiz For Skin Station

2007-07-20T23:37:00.000+08:00

Observe and comment the skin findings.

What are your differentials?

Fundoscopy Quiz

2007-07-15T22:21:00.002+08:00

Wuchereria got this for his PACES Singapore exam last year.

What is your diagnosis?

History - Quiz Chest Pain

2007-07-04T15:14:00.000+08:00

The most failed station according to a PACES book is Station 2 - History because it is the least practiced for the exam station. We were discussing about this a moment ago.

Scenario : Mdm Ma is a 40 years old Malay lady who has been diagnosed hypertension and is currently on T. Metoprolol 25 mg bd. The GP has referred this case as this lady has been complaining of chest pain for the past 6 weeks.

Kindly take a history from this patient.

Based on the history,

This lady had the following characteristics of chest pain - crushing, radiating to the back, lasting for 5 minutes, at rest, almost everyday, not related to meals or respiration. No DM, Stroke. Strong family history of IHD - Father IHD at 60 y.o, Brother IHD - passed away at 45y.o and grandmother IHD at 71 years old. Non-smoker, no alcohol consumption. Works as a clerk, married with 4 children.

This is the very brief history.

Questions

What are the provisional diagnosis in this case ?
What is the differential diagnosis in this case and so with the differential diagnosis, and what are the further questions you would like to ask ?
What investigations and plan ?

Some Drills On Station 5 (Part 4)

2007-07-03T16:34:00.000+08:00

Station stem: Please examine this lady's hands and proceed accordingly.

1) What is your diagnosis?
2) What other systems would you like to examine?
3) How would you treat this lady?

Quiz CVS

2007-06-29T23:47:00.000+08:00

A consultoid cardiologist took me for a short case 1 hour ago.

This man had a clear cut mitral valve replacement ! However the question was what was the other scar due to ??

Any takers ?

IE Update

2007-06-25T01:19:00.000+08:00

This gentleman presents with fever for 3/52. Please Ex his cardiovascular system

I would like to complete my Ex by checking
1) fundus – Roth spot
2) Dipstick the urine for hematuria
3) Temperature chart
4) Abd- spleenomegaly

This gentleman looks thin and he has a brannula at his right wrist. He has stigmata of IE as evidenced by presence of Osler nodes and Janeway lesion. There is no finger clubbing or splinter haemorrhage. There are also IV puncture marks over the cubital fossa.
PR is 90 bpm regularly regular. There is no radial-radial delay and the pulse is not collapsing.
He is pink and not jaundice.
Jugular venous pressure is not elevated.
Apex beat is not displaced and there is no thrill or Left parasternal heave.
There is a PSM best heard at the apex and non radiating

This gentleman has IE currently not in failure. He probably is an IVDU in view of the presence of IV puncture marks.

Ix:
1) FBC- WCC, normochromic normocytic anaemia
2) ESR
3) Blood C&S- 3x fr different sites over 1 hour time span
4) ECHO

Mx
1) Antibiotics- IV C. Pen + Genta x 2/52
IV Cloxa + Genta x 2/52 until review C&S
2) Surgery if
a. Persistent Blood C&S/ relapse
b. Abscess
c. Fungal
d. Damaged valve
e. 2nd / 3rd degree heart block secondary to aortic valve vegetation
f. New aneurysm of the sinus of Valsalva

IE prophylaxis for Dental Procedure(Circulation May 8 2007)

1) Prosthetic heart valve

2) Previous IE

3) Congenital heart disease

4) Cardiac transplant patients who develop valvulopathy

give oral amoxy 2g, 30 min before dental procedure

Prophylactic antibiotic for IE not recommended for GU/ GI tract procedure

An Approach To Bilateral Partial Ptosis (Part 1)

2007-06-23T13:35:00.000+08:00

The usual stem of CNS station would be:
Examine this patient's cranial nerve.

It would be lucky if on inspection, there is obvious partial ptosis. The immediate next step would be thinking of the following 3 possibilities:

Is it bilateral Horner syndrome?
Is it bilateral 3rd CN palsy? (Rather unlikely to appear in real exam if it is due to central cause rather than peripheral)
Is it neuromuscular weakness?

Our Part 1 will concentrate on neuromuscular weakness
During CN examination, we have effectively ruled out Horner and CN III palsy. So, it is likely partial ptosis due to neuromuscular weakness. At this point, there should be at least 5 differential diagnosis in our mind:

Myasthenia Gravis/ LEMS
Gullain Barre Syndrome (Miller-Fisher)
Dystrophic Myotonia
Fasciomusculoscapular dystrophy
Oculopharyngeal Muscular Dystrophy

Brothers with Dystrophic Myotonia

Therefore, at the end of CN examination, we need to do something extra to get the most likely diagnosis. Do as follow:

Check for fatiguability (eye lids, upper limbs, nasal speech)
Check for thymectomy scar (may be hidden by patient's dress, and it would be fatal for missing the scar)
Check for diplopia on extreme gaze
Check for myotonia, by percussing the thenar muscle, and ask patient to grip hands
Check lower limb reflex for areflexia in GBS
Check for winged scapula

During presentation, we need to mention about the possibility of medical emergency, in this situation, we should mention:

"I would like to complete my examination by requesting a bed side spirometry to assess for respiratory mucle weakness" -for suspected Myasthenia/LEMS/GBS
"I would like to examine upper and lower limb for ascending weakness and aflexia" -for GBS

In view of the complexity of each disease, it would be rather less possible to discuss each in details. Maybe in next few sessions....

Related posts:
Ptosis for PACES 1
Ptosis for PACES 2

Gait Quiz 2

2007-06-23T00:18:00.000+08:00

Observe and describe the gait. Then, proceed with the necessary neurological examination.

Agenda For PACES Communication

2007-06-18T23:33:00.000+08:00

Samad shared some useful tips for communication station in PACES forum.

Almost all the examiner I talked to put lot of stress on 'setting the agenda' for history taking & communication:

Your introduction with designation
Your role in management
Check the identiy of the patient & relative if said so in the scenerio
Set the agenda i.e why is this meeting
Will be willing to answer all questions
No hasty gesture i.e we have 10 minutes etc, if time finishes can say I feel a few issues needs to be addressed to will make another appointment within a few days.
Always, always- summarize

Anything to add from the peers?

Some Drills On Station 5 (Part 3)

2007-06-17T21:18:00.000+08:00

This series of photos belongs to a lady who presents with a rash.

The registrar in-charge in the PACES centre would be too happy to include cases like this in station 5, if they happen to land up in the ward at the right timing :)

State your diagnosis and the differential causes.

How would you manage this lady?

Gait Quiz

2007-06-16T23:44:00.000+08:00

The responses for quiz series so far are great! Hence, I decided to post a video demonstrating a gait disorder.

Here, it goes.

This is the neurology station. Please observe the gait.

What type of gait is this man demonstrating?

How would you proceed with the necessary neurological examination?

Video contributed by Wuchereria

Fundoscopy Quiz

2007-06-15T14:41:00.000+08:00

Yesterday, a consultant neurologist came to my hospital and took one of the PACES candidates for a mock.

This was what the patient had(picture above). It was Station 5 Fundoscopy.

Quiz :

1) What is your diagnosis ?

2) What else would you look for ?

3) What are the common causes ?

4) What would you look for in the other eye ?

The patient was a young lady.

What is your complete diagnosis ?

Station 5 Quiz

2007-06-14T11:49:00.000+08:00

Thank you for the great response for the 1st Quiz.

Here comes the quiz for Station 5.

The diagnosis is rather clear cut but how do we get 4/4 instead of 3/3 ??

This patient has acromegaly and the disease is inactive, currently complicated by bilateral carpal tunnel syndrome and urinary tract infection
Examination of the hands reveals large spade like hand. It is however not sweaty or warm. Positive Tinel sign suggestive of bilateral carpal tunnel syndrome.
There is no proximal muscle weakness
There is prominent supraorbital ridge with prognathism and large nose and large tongue. There is also interdental separation.
There is no visual field defect and no goiter.
There is heel pad thickening

I would also like to check the BP, urine dipstick for glycosuria, organomegaly and the old photograph of this pt.

There are several other signs which are not listed here which may need to be checked. Please identify and tell so that one can score 4/4 !

Any takers ?

Pictures and case contributed by Wuchereria.

Respiratory Quiz

2007-06-13T12:57:00.000+08:00

During yesterday’s MRCP mock exam, Wuchereria had a tough time with one of the local examiner.

This patient has clubbing with cyanosis and bilateral fine crepitations over the bases with a scar as seen in the picture. He also has an area of consolidation over the R lower zone

Examiner : How do you correlate the scar and the findings ?

Any takers?

This case is contributed by Wuchereria.

SVC Obstruction

2007-06-11T23:43:00.000+08:00

There is prominent veins over this patient's anterior chest wall. They are tortuous and dilated. The neck veins are engorged with loss of pulsation. The face looks plethoric and suffused.

This is superior vena cava obstruction.

This patient has undergone recent radiotherapy for this medical emergency condition as evidenced by fresh radiation ink marks and skin erythema over the same area.

Any other signs to mention? How do you tie them up to form a complete diagnosis?

What are the other clinical clues to the unifying diagnosis?

Photo courtesy of Wuchereria

3rd IMU-HTJ MRCP PACES Preparatory Course

2007-06-10T14:12:00.000+08:00

I have chance to attend the 1st IMU PACES course in September 2005. Personally, I think it is specially designed for those who are intending to take PACES in Malaysia or Singapore. It is well organised with wide range of PACES cases. Everyone has chance to present to some of the prominent local PACES examiner.

I would say it is one of the best PACES course one can get in Malaysia! In short, it is highly recommended for every local PACES candidates!

So, quickly register as the places are limited especially the MOCK exam.

Venue: Clinical School, International Medical University,
Jalan Rasah,
70300 Seremban,
Negeri Sembilan.

Date: 6 - 8 September 2007

Cost:

a.RM 800 (PACES course without MOCK Exam)

b.RM 1,000 (inclusive of MOCK Exam)

Contact Person:
Danielle Ho
Postgraduate Studies and Research
International Medical University
No. 126, Jalan 19/155B
Bukit Jalil
57000 Kuala Lumpur
Tel: +603-8656 7228 (Ext. 2212)
Fax: +603-8656 7299
Email: danielle_ho@imu.edu.my
http://www.imu.edu.my

Fasciculation = MND

2007-06-09T21:07:00.000+08:00

What do fasciculations mean in PACES station? One of the prominent lecturer from my university once said, it is equivalent to anterior horn cell lesion until proven otherwise in PACES (or even in clinical practice)!

In the above movie, the patient has fasciculations (spontaneous contraction of a motor unit) noted in the deltoid muscle as well as atrophy. There is also atrophy of the small muscles of the hands. These findings can be seen in motor neuron disease such as amyotrophic lateral sclerosis.

Movies drawn from the Neurologic Exam and PediNeurologic Exam websites are used by permission of Paul D. Larsen, M.D., University of Nebraska Medical Center and Suzanne S. Stensaas, Ph.D., University of Utah School of Medicine.

High Stepping Gait

2007-06-04T20:24:00.001+08:00

High steppage gait occurs due to foot drop where dorsiflexion of the foot cannot occur. The knee is flexed and raised to allow the foot to clear the ground. It occurs in L4, 5 root lesions, common peroneal lesions, peripheral neuropathy. Occasionally it may be due to lesions in the motor cortex.

This patient has right foot drop due to a common peroneal nerve lesion.

Video contributed by Wuchereria

Abdomen: Thalassemia

2007-06-03T21:30:00.001+08:00

This 20 year old young man was referred from our paediatric colleagues for further follow up and management. Please examine his abdominal system.

Suggested presentation
(When turning to the examiner)

I would like to complete my examination by examining his genitalia, doing a per rectum examination.

(If asked to present your findings)

This thin young man is pale, jaundiced, hyperpigmented and short for his age. He has frontal bossing, prominent maxillaries and chipmunk teeth which are maloccluded. There is also sparse axillary and pubic hair

The abdomen is distended and there is a left lower quadrant scar. There is hepatomegaly, extending 4 finger breadths beneath the costal margin. The liver has smooth edges and non tender on palpation. The kidneys are not ballotable. There is no shifting dullness to suggest the presence of ascites.

I did not find any lymph nodes in him. There were no features to suggest chronic liver failure. I also note he does not have any abdominal puncture wounds to suggest the use of desferral

In summary, this is short young man with jaundice, pallor, hepatomegaly, a previous splenectomy done and has thalaessaemic facies and possible underlying hypogonadism and haematochromatosis. He has chronic hemolytic aneamia. He is transfusion dependent.

I would like to offer the differential of a haemoglobinopathy. The most common haemoglobinopathy in this part of the world is Thalaessaemia.

Quenstions
1.What investigations would you like to do?
I would like to confirm the underlying cause of hemolytic anemia by doing serum electrophoresis. I would like assess the complications of treatment and patient’s disease by doing LFT, coagulation profile, hormonal assay, hepatitis serology and echocardiogram. I will assess his functional status using FBC.

2.How would you like to manage this young man?
a. Treatment of Disease- hypertransfusion, Splenectomy, Pneumococal vaccination, bone marrow transplant in some centres
b. Treatment of its complications-hormone replacement therapy, iron chelation therapy, control heart failure
c. Patient and family education, genetic counseling is also important so that family members can be screened and treated early.

Contributed by Giant Eagle

Excellent Eye Simulator

2007-06-02T09:59:00.001+08:00

Eye Simulator/Virtual Patient Simulator
Spotted this Eye Simulator posted in MMR site. I tested it myself. It's great. It demonstrates most of the pupillary defects that a MRCPian need to know.

Go, go, go and test it out now!

Many thanks to Rick Lasslo,M.D.,M.S., Gary Henderson, PhD, and John Keltner, M.D. from UC Davis School of Medicine who developed this eye simulator.

Cerebellar Gait

2007-06-02T00:36:00.001+08:00

Instruction: Tests this patient's gait.

Presentation:
The patient has a broad-based gait. He is unable to perform tandem walking.

Proceed as follows:
Tell the examiner that you would like to examine the patient for other cerebellar signs.

Source: Wright State University

PACES Window!

2007-05-31T21:00:00.000+08:00

One of the station that most PACES candidate fear is fundus station. In this station, our fate is dependent on the small window i.e. pupil. I had a bad experience during PACES exam as the patient's pupils were not well dilated during my PM session. Later, I only learnt that the pupils will only be dilated once in PACES. So, if you do get a "small window", remember to commend that your examination of the fundus is suboptimal.

I found a visual guide on fundocopic examination by California State University. Hope it helps.

EYES ARE THE WINDOW TO THE SOUL

2007-05-31T07:34:00.000+08:00

This gentleman presented with giddiness. Please look and proceed

I would like to complete my Ex by checking the fundus for papilloedema or optic atrophy, corneal reflex and the gag reflex. I would also like to Ex the UL and LL for pyramidal signs and finally measuring the BP.

This gentleman has Left Internuclear Opthalmoplegia where by the Left eye is unable to adduct and the right eye has nystagmus with the fast phase towards the right side upon looking to the right. The rest of the cranial nerves are intact.

I would like to consider causes such as stroke or demyelinating disease.

Examiner : What are the other causes of INO?
Pan : Tumour, Drugs such as phenytoin and carbamazapine

Examiner : Where is the lesion?
Pan : Left Medial Longitudinal Fasiculus (connecting 3rd nerve nucleus to
the opposite 6th nerve nucleus) at the brain stem

Examiner : How would you like to investigate this pt?
Pan : I would like to request for a MRI of the brain.

MRI came back as small left pontine infarct

Romberg's test

2007-05-30T22:29:00.000+08:00

The 1st part of the video clip clearly demonstrates positive Romberg's test. The patient is losing his balance upon closing his eyes. Please take note that the test is considered positive only when patient is about to fall. So, please guard the patient when perfoming this test.

The 2nd part shows Stamping gait - broad based, foot stamping on the floor.

When is the lesion?
-It is seen in propioceptive disorders. The lesion is in the peripheral nerve or posterior column.

What is the lesion?
1.Peripheral neuropathy - DM,Alcoholism, Vit B12 deficiency etc
2.Tabes dorsalis
3.Subacute combined degeneration of the spinal cord (SACD)
4.Friedreich's ataxia

Is Scar Really A Gift?

2007-05-23T13:21:00.000+08:00

Well, to answer this particular question, I'll illustrate it with my PACES case. As I've shared earlier on of my neurology case in station 3, this would be the continuation of what had happened after that.

The same pair of nice examiners had ushered me into another room.

An elderly gentleman had already been properly exposed and positioned propped up at 45o.

"Please examine the cardiovascular system and tell us your findings."

Again, a rather simple stem. Nothing fancy.

I quickly noticed a midline sternotomy scar on the patient. I gathered my clinical experience and in my mind, I had these possibilities outlined:

Patient had a valve replacement done, either metallic or bioprothetic - this is by far the commonest scenario encountered in PACES with sternotomy scar
Possible valve repair
Patient had a CABG done - ?evidence of venous harvest
Patient had sternotomy for excision of cardiac tumours or masses eg, atrial myxoma, resistant IE etc or closure of large septal defects
Sternotomy for non-cardiac surgery eg, thymectomy, repair of other midline structures etc. - this is highly unlikely in PACES station 3!

I proceeded to pick up his hands and started examining the peripheries. The only positive sign was of an irregularly irregular pulse at about 60-70bpm. There were no stigmata of IE and in particular, I could not see any scar of previous venous harvest both in the upper and lower limbs.

He was pink on air and there was no jaundice. The venous pressure is not elevated and, as mentioned earlier, there was a midline sternotomy scar which was well healed. There was no scar elsewhere at the precordium.

At this juncture, I gathered that the positive signs were:

Rate-controlled AF
Midline scar

I told myself that I should be looking hard for a mitral valve pathology hence needing surgical intervention, with the distant possibility of a previous large ASD now closed.

On examination of the precordium, the apex beat is not displaced. There was no thrill. The were no signs of raised pulmonary pressure. The first heart sound was loud and the second heart sound was well heard. There were no other added sounds. There was no signs of cardiac failure and no signs to suggest overwarfarinisation.

"So what do you think?"

"I think this gentleman has had a mitral valve replacement done, complicated by atrial fibrillation currently rate-controlled. There was no signs of cardiac failure. There were no metallic sounds heard on auscultation and hence it cannot be a metallic valve. It is possible that this gentleman has had a bioprosthetic mitral valve implanted."

"Are you sure? What would be the other possibilites?"

"It is still possible that he had a mitral valve repair done previously."

"Which one do you think is more likely?"

"I think a valve replacement would be more likely as the presence of atrial fibrillation would indicate the chronicity of the mitral valve pathology, which is, mitral stenosis in this case in view of the undisplaced apex beat. A valve repair is usually being employed to ameliorate a less severe or chronic valve pathology."

"Ok then, you say that it is a bioprothesis. Would you still want to give this patient warfarin?"

"Yes. I would like to anticoagulate this patient for the indication of atrial fibrillation."

"Why is that so?"

"To reduce the risk of thromboembolism. Warfarin is shown to be superior than aspirin alone in preventing thromboembolism, for example stroke, which causes significant morbidity and mortality."

"Do you know the percentage of thromboembolic risk reduction by giving patients warfarin?"

At this time, the bell went.

Verdict: 4/3

Parkinsonism

2007-05-22T20:50:00.000+08:00

Undoubtedly, some of the signs in PACES is more presentable in video format.I managed to fish out some videos from YouTube database to share.

This video shows resting tremor and pill rolling of the thumb.

The face is expressionless and the gait is festinant with stooping posture and lacking of bilateral arm swings.

A Neck Scar In Abdomen Station

2007-05-22T17:57:00.000+08:00

Parathyroidectomy scar is smaller than thyroidectomy scar.

It is located higher than post-tracheostomy scar (sternal notch).

Here is a post by Experience in PACES forum.

"Abdomen station: Examiner introduced a middle aged thin lady having tiredness and SOBE."

I introduced myself, positioned and stood at the foot side. She had sallow complexion, a midline / right iliac fossa and right lumber scar on the abdomen. Examination of hands was unremarkable. On left arm there was a AV fistula with palpable vibrations/hum. Above this was a small scar. She had pale conjunctiva. A transverse about 3cm scar on the thyroid. On abdominal palpation there was palpable and ballotable mass 15cm x 6cm with irregular surface in left lumber region. No other masses were palpable in the abdomen and there was no venous hum on auscultation. No sacral or pedal oedema and there were no lymph nodes anywhere. I expected a transplant in LIF scar but there was none.

Examiner asked what is the diagnosis after I presented the case. I said 'These findings are suggestive of APKD and patient has right nephrectomy. She has ESRF and is on renal replacement therapy'

Only then, examiner reminded me of thyroid scar and asked is it related to her present condition. I was stressed since the scar was much smaller than usual thyroidectomy scar. Then I suddenly realised that this patient had 'parathyroidectomy' and a small scar on the left arm was due to one of the parathyroid transplant in the arm.

Take home messages:
1. Neck scar in abdomen station = suspected parathyroidectomy scar
2. Be prepared to recognise the reasons behind the scars in abdomen station

Doc, Every Second Of My Life I Am Dizzy

2007-05-21T23:00:00.001+08:00

I am still working in neurology department, still seeing a lot of referrals from the northern region of Malaysia. I was referred a patient from an orthopedic surgeon for difficulty in walking TRO spinal cord compression. The surgeon had done a MRI 0f thoracic and lumbar region which turned out to be normal.

The case mentioned is a 45-year-old Chinese man, working as a mechanic. I remembered he kept on complaining of dizziness from the moment he stepped into my clinic. To cut the story short, he had been having severe dizziness and imbalance gait for nearly 2 years. It was progressively worsen for the past 3 months before he sought treatment from medical doctor. Functionally, he was terribly disabled by those symptoms.

On examination, he was ataxic and hardly able to stand or walk steadily without any assistance. There was bilateral cerebellar signs as evidenced by presence of dysmetria, intentional tremor and failure of performing rapid alternate motion test.

There was obvious nystagmus demonstrated bilaterally. He had staccato speech. Further examination revealed that the lower limbs were hypertonic and hyperreflexic. Clonus was present with bilateral upgoing plantar responses. His sensation of pain and propioception was intact.

In conclusion, he has bilateral cerebellar signs with UMN signs to suggest corticospinal tract involvement.

The possible diagnosis that should be considered in this case:
1. Spinocerebellar ataxia (SCA)
2. Multiple sclerosis

How should you proceed to reach the diagnosis?
What is the investigation of choice at this stage?

Any comments?

Related post

Absolute Manna From Heaven - A Renal Case, Examine This Pt's Abdomen

2007-05-19T08:01:00.000+08:00

This case was one I got during my mock , A 56 yr gentleman of Asian descent, he had warty fingers , looked pale peripherally, with an oblique scar in RIF,a palpable mass which is dull to percussion below it .Another scar on the left lateral aspect of the abdo extending all the way to the back, a scar of about 3cm just below the umbilicus, 2 symmetrical scars just above the bikini line oneither side, had a non working brachio-cephalic fistula on the left,a non-working radio-cephalic fistula on the left, scars of previous perma-cath on rt pectoral region, moon face, buffalo hump,had gum hypertrophy,centripetal obesity with no ascites.

I think from this you can visualise my patient, he had all the signs, but you needed to put them in order to make a good perfomance, This time I went for the jugular:

Mr XYZ has ESRF and has had a renal transplant in the RIF which is working well,He has gum hypetrophy which evidence of previous Cyclosporin use and warty fingers which is evidence of previous Azathioprine use.He also has a buffalo hump and centripetal deposition of adipose tissue which is evidence of long term steroidal use.He has previous scars from Tenckhoff catheters for peritoneal dialysis. He has also had haemodialysis using the permacath and from abrachiocephalic fistula which is no longer working, He has no ascites and his abdomen is non tender

I would like to comlplete my examination by checking Temp chart, BP, urine dip for glycosuria, fundoscopy

Q: What do you think is the cause of renal failure
A:Being of Asian descent Diabetes is highest on my list but could also be due to hypertension, glomerulonephritis, adult polycystic kidney dse, nephrocalcinosis

Q: You mentioned about all scars except one on the left abdo , what was it for?
A: Maybe some unrelated abdo surgery, or complications from CAPD or left renal surgery.

Q: Can you tell us the indications for nephrectomy in APCKD?
A: Very large kidneys, recurrent abdo pain, recurrent haemorrhage into cysts and malihnant change

I later found that this pt had APCKD and had undergone lt nephrectomy with RIF transplant

Talk To This Lady And Proceed

2007-05-07T13:37:00.000+08:00

This was the station 3 stem when I took my PACES in London. Short stem but luckily I was well prepared for what was in store;)

This was the last station of the day, and trust me... the adrenaline surge was quite intense. The pair of nice gentlemen had me ushered in the room with a lady sitting on a couch. I immediately noticed a walking stick beside her. She was of medium built. I looked hard for clues of clinical syndrome such as dystrophia mytonica or FSH but I'd found none.

Pondering the station stem, I had these possibilities outlined in my mind:

Cerebellar syndrome - young lady with walking stick, must consider gait abnormalities. Differentials to consider: FA, SCA, MS, ?Wilson and other infiltrative disorders
Bulbar or pseudobulbar palsy - Differentials: MND, ?young stroke
Parkinsonism - unlikely PD in young lady. Differentials: drug use (neuroleptics), ?substance abuse

I proceeded to talk to the patient. To be honest, it didn't strike me to be of anything abnormal for a moment. Luckily, I stayed with the locals for 3/52 prior to the exam and hence could appreciate the subtle slurring and staccato'ing. It wasn't very clear even with phrases like "British Constituition" or "Hippopotamus"!

At this jucture, the examiners interrupted me: "So what do you think?"

I gathered my thoughts and quickly said: "I've noticed very subtle scanning speech and staccato speech. I would like to proceed to examine the cerebellar system fully."

"Please do."

I proceeded to elicit every cerebellar sign that I could. The lady had obvious past-pointing, more on the right side and dysdiadochokinesia. However, truncal stability was relatively preserved. There was sustained nystagmus on looking to the right. She displayed broad-based gait with failure to perform tandem walk. The Rhomberg's sign was negative.

I was happy to conclude that she had ample of signs to suggest a cerebellar syndrome, with the possible underlying etiologies being MS (young lady and in temperate region), and hereditary ataxias such as SCA or FA. I would complete the examination by looking into her fundi for optic atrophy as well as to examine the lower limbs for long tract signs.

"If you are given an opportunity to ask one question, what would you ask?"

"I would elicit history of similar illness running in the family."

"Please do."

I proceeded to ask the nice lady with the question and I found out that her mother and the elder brother had the same condition.

"So what do you think?"

"The inheritance pattern is likely of autosomal dominant type, and hence it cannot be Friedrich ataxia. I would think this patient has spinocerebellar ataxia of autosomal dominant type."

The examiners nodded and smiled: They tossed me a few more questions on the other possible causes of cerebellar signs in a young lady before concluding the station.

"Now let's get on to the cardiovascular station."

Verdict: 4/4

I Can't Feel Yer Pulse!

2007-04-30T19:19:00.000+08:00

Recently, I had the privilege to be invited as an MRCP PACES mock examiner in one of my local hospitals. It reminded me much of my days when me and my few close comrades were striving to perfect our clinical skills and to embark on the MRCPian journey.

I must say that it was a very 'close to heart' experience, as I truely shared the bitterness and joy shown in the candidates.

Amongst the cases, the toughest (being most elusive) one is a young boy with the following station stem.

Station 3: Mr K is admitted with uncontrolled hypertension. Please examine the cardiovascular system.

I would complete my examination by measuring his blood pressure on both sides.
Examiner:"The blood pressure is 170/100mmHg on both sides."

The principal findings on this young man are radiofemoral delay with absent lower limbs distal pulses. I could not feel the posterior tibial and dorsalis pedis pulses on both sides, though the popliteal pulses were feeble. There were no puncture marks or haematoma on the groins to suggest a recent intraarterial procedure. Examination of the precordium revealed no abnormalities, in particular, there is no murmur to suggest an intracardiac shunt or aortic root abnormalities. There was no scar seen. There was no sign of heart failure.

With the aforementioned findings, I think this young man has coarctation of aorta complicated by uncontrolled hypertension. It would be most pertinent to look for signs of target organ damage urgently, ie preliminarily funduscopy, urinalysis and serum creatinine. In view of his age, I would also consider the differential diagnosis of Takayasu arteritis.

The verdict:
All candidates who were given this case failed to elicit the delay in pulses. Frankly, I don't think anyone would hardly miss the diagnosis if it's a normal daily clinic case. Young hypertensives... there are only a handful of conditions that can be presented in a PACES short case station!

Station 5 - Acromegaly, Uneasy To Get "4" For An Easy Diagnosis

2007-04-30T11:27:00.000+08:00

During my singapore PACES exam, i got an acromegaly case. The stem being " please examine the patient's hands".

By one look at the patient, we are happy to conclude that the patient has acromegaly, the next thing in my mind is what the examiner want me to pick up from the patient's hands with acromegaly.

Possible things to pick up:
1) Carpal Tunnel syndrome
2) Osteoarthritis
3) Pure hand feature of acromegaly

We may easily get a 4 mark if we follow the stem, go accordingly to point out the features that support the diagnosis.
Steps to follow in order for acromegaly patient in the very moment of 2 min before we use up 3 min for presentation.
1) Hand : large spade like hand, doughy hand, sweaty palm, tinel's sign

2) armpit: especially to look for skin tag (most candidate miss it, and we may only get 3 if we miss it)

3) Face: Prominent supraorbital ridge, prognatism, widely-space teeth, macroglossia, increase in skin creases/ wrinkles

4) Visual field assessment -bitemporal hemianopia

5) Lower limb: large foot, osteoarthritis of knee, thicken heel pad

6) complete by mentioning: checking BP, urine for glycosuria, examine for galactoria

Present as such order to make it systematic but the opening sentence must be base on the stem, in this case, "examine the hand"
Eg:
This patient has features of acromegaly. I say so because she has a large doughy, spade like hand. Her palm appeared sweaty. There is evidence of carpal tunnel syndrome as the tinel sign is positive. I found a skin tag over her right axillary area. Her voice appears to be coarse, she has prominent supraorbital ridge, and prognatism. She has macroglossia with widely-space teeth. Her foot appears to be large. Her heel pad is thickened. There is sign of osteoarthritis over her knee joint. There is no evidence of bitemporal hemianopia.

In conclusion, Mdm X has acromegaly. The most likely cause is a macroadenoma. There is sign of active disease in view of presence of sweaty palm, and skin tag. I would like to further assess her cardiovascular system.

These are the questions the examiner asked from me: ( not much time left after my presentation)
1) How do you confirm the diagnosis
Answer: Failure of suppression of GH level to less than 2ng/ml after oral glucose confirm the diagnosis

2) What further test you want to do?
Answer: Localization of pituitary tumour by requesting a MRI of brain

3) What are the treatment?
optimization of cardiovascular risk by strict BP and sugar control, refer eye for Visual field perimetry, definitive treatment: transphenoidal hypophysectomy, medical: somatostatin analogue: Octreotide, GH receptor antagonist: Pegvisomant

That end the session with clear pass from both examiner.
Further possible question:
1) What other source of GH if MRI shows no macroadenoma?
Answer: ectopic growth hormone production, small cell CA lung

2) How do you monitor treatment response?
Answer: insulin like growth factor

3) Do you know of any endocrine adenoma association with acomegaly?
Answer: MEN type 1 -parathyroid hyperplasia, pituitary adenoma, pancreatic tumor
Need to examine calcium level

Breaking Bad News 1

2007-04-27T20:55:00.000+08:00

Inform brain death and withdrawal of treatment

Mr Smoki is a 65 y.o. gentleman admitted 3 days ago for acute exacerbation of COPD. He has been getting dyspneic for past few days, with fever and increased sputum production but has refused for admission. He was found collapsed by her daughter, but resuscitation team has managed to resuscitate him and was sent to hospital. He has history of recurrent admission for COPD. For the past 1 year, his COPD symptoms worsened, and he required 5 x admission for the past 1 year. He has been stopped smoking 3 months back due to progressive worsening dyspnea. He has been staying with his only daughter, and his wife has passed away due to myocardial infarct. His daughter Miss Norsmok has been quite supportive of her father so far, and has been spending her time all along during these hospital stay.

There has been no improvement in his father’s condition throughout the ICU stay. He has spiking fever and it was complicated by septic shock and multi organ damage. His blood pressure has been low, an now require inotropic support. The ICU team has discussed poor prognosis to medical team. Brainstem test was done, and Mr Smoki was confirmed brain death. Therefore, withdrawal of treatment is imminent.

You are the senior medical officer in charge appointed to meet Miss Norsmok. Your task is to explain braindeath to her and discuss the issue of withdrawal of treatment.

1) Introduction
Dr: Im Dr X, im here to discuss with you about your father’s condition. Do you have anyone coming along for the discussion?

Miss Norsmok: No, I came alone.

2) Explore how much she knows about her father
Dr: How do you feel about your father’s condition? Did anyone tell you about your father’s condition before?

Miss N: Nobody so far tell me in detail. But I was told that my father is critical. Doctor, did anything go wrong?

3) Explaining general condition
Dr: Im afraid we have bad news for you. Your father has been admitted with severe lung disease. We have to protect his lung into rest. His breathing is supported by our machine. It has been hard for your father to recover in view of his severe lung disease. Your father’s condition was worsened by multiple organ failure due to severe infection. We have been trying our best but we failed to do so. (give a pause…)

Miss N: What do you mean? Fail?

Dr: Yes. The fact is hard to accept, but we have perform a test and have found that your father has brain death, in other word, your father has passed away. We are sorry.

Miss N: It can’t be. He is still breathing, and he still have pulse..Are you sure my father has died?

Dr: Yes. Your father would not be able to breath by his own. It is the machine which help his breathing. And his pulse is due to medication, which temporally make his heart beat. Without artificial support, his heart will stop beating, and he would stop breathing. Therefore, your father has passed away.

Miss N: I can’t believe it…(pause…)

4) Discuss withdrawal of treatment

Dr: You seems upset by the news. I could understand that. It is difficult for us to discuss this at this moment, but I need to tell you that we are going to withdraw treatment to your father. How do you feel about it?

Miss N: Are you going to give up on my father? Do you mean you want to let my father stop breathing?? Don’t ever mention it!

( Do not be panic as most family would think that we are going to let the patient die. We need to confer to them that her thought is incorrect)

Dr: Miss Norsmoke, we never give up treating your father. It is however not appropriate to continue treatment in your father, as he already passed away. I’m sorry about this, and I know that you need time to accept.

Miss N: …What are you going to do Dr?

Dr: We are going to stop the medication that support the heart as well as stopping the machine. Your father would stop breathing and his heart beat would stop in a short moment. There would be no suffering to your father as he has already passed away. (Mention the word “passed away” few times to remind the family about the death)

5) Explore reason if disagree
Miss N: No, I don’t want you to do that. You cant stop the treatment.

Dr: It must be hard for the decision. But can I ask why do you think in such a way? Do you have any religious believe in this matter? Did your father ever express his will about how he would be treated before this?

Explore the reason and sort out any misconception is utmost important. Decision of the relative must be regarded important, although decision of withdrawing treatment lies in the hand of clinicians.
Miss N: No, there is no specific reason. I don’t accept that my father be treated as such.

Dr: Withdrawing treatment may be unfamiliar to most people. I would address the issue to my consultant. In a short while, we would have another discussion with my consultant. Do not hesitate if you have any question regarding the problem. See you again.

Issue and Discussion:

Autonomy
Beneficence
Nonmaleficence
Distributive justice

Why withdraw treatment?
1) Withdrawal of treatment is an issue in intensive care medicine because it is now possible to maintain life for long periods without any hope of recovery.
2) It is often easier to withhold a treatment than to withdraw it once it has been instituted. Ethically, however, there is no difference between withdrawing a treatment that is felt to offer no benefit and withholding one that is not indicated.
3) About 70% of deaths in intensive care occur after withdrawal of treatment. This is not euthanasia. The cause of death remains the underlying disease process, and treatment is withdrawn as it has become futile.
4) In general, treatment is withdrawn when death is felt to be inevitable despite continued treatment. This would typically be when dysfunction in three or more organ systems persists or worsens despite active treatment or in cases such as multiple organ failure in patients with failed bone marrow transplantation.

Patient autonomy
1) Autonomy is another of the basic precepts of ethical practice, but there are problems with its implementation in the intensive care unit. Most critically ill patients are not competent to participate in discussion because of sedation or their illness.

2) in the United Kingdom relatives do not have legal rights of decision making

3) Another difficult issue occurs when a patient may survive but with a poor quality of life

4) Relatives must be kept fully informed about the patient's condition, in particular regarding issues of limiting and withdrawing treatment.

5) Although decisions rest with the medical staff, it is unwise to limit or withdraw treatment without the agreement of the relatives

Problems
1) The referring team request continued futile therapy
This can usually be resolved by explaining the rationale and offering a second opinion from another intensive care consultant. If conflict still remains, treatment cannot be withdrawn. The family should not be informed of a decision to withdraw that is then rescinded because of interteam conflicts. It will reduce their faith in subsequent decisions and undermine confidence in the predicted outcome.

2) The patient's family requests continued futile therapy
Guilt usually plays a part in the family's request to continue treatment, although religious and cultural factors may also contribute. Agreement can usually be obtained by explaining the rationale again and offering a second opinion from within or outside the intensive care team. It is best not to withdraw treatment if there is conflict. However, the final decision rests with the intensive care team. This underlines the need for good communication.

3) The family requests inappropriate discontinuation of therapy.
The rationale behind the therapy and the reasons why continuing treatment is thought appropriate should be explained. The duty of care is to the patient, not the family. Again, a second opinion can be offered.

4) The patient requests discontinuation of therapy.
Explain to the patient the rationale for the treatment and that, in the opinion of the intensive care team, a chance of recovery exists. It may be appropriate to offer a short term contract for treatment (for example, 48 hours then review). Ultimately, the competent patient has the right to refuse treatment even if that treatment is life saving.

Pseudohypoparathyroidism

2007-04-21T15:31:00.000+08:00

The stem

This 30year old lady was noted to be short by the polyclinic MO. Would you like to examine her?

Suggested presentation

This young woman is overweight, short, with rounded facies, missing teeth, short fingers and a short neck. She also has shortening of both fourth metacarpals.

The combination of these features suggest the diagnosis of psedohypoparathyroidism type 1a

I would like to elicit Chvostek’ and Trosseau’s sign as she may have hypocalcaemia.

Questions that may be asked

What is the basic abnormality in Type Ia patients?
Ans. There is target organ resistance to the action of parathyroid hormone. The defect occurs proximal to the formation of the second messenger , cAMP

How will you treat this patient?
Ans Acute symptomatic hypocalcaemia can be corrected with infused calcium
Gluconate with cardiac monitoring to prevent hypercalcaemia. For long term
treatment, use of calcium supplements and activated Vitamin D to keep calcium
levels within the normal range. (Activated Vit D eg calcitriol to increase
absorption of Calcium in guts and increased retention in kidneys)

What biochemical test can you do in this patient
Ans. Ellsworth Howard Test. In a normal person, infusion of parathyroid hormone will cause a rise in urinary phosptate and cAMP excretion. In Type I A patients, there is no increase in urinary cAMP or phosphate.

What are other causes of short stature you know of?
Ans Genetic for example familial, achondroplasia, Turners and Noonans and Downs syndrome
Nutritional or general illness during childhood eg low birth weight, congenital heart disease or renal disease

Contributed by Giant Eagle

Expect The Unexpected

2007-03-18T13:05:00.000+08:00

Opthalmoplegia

Puan Rahimah complains of giddiness. Please look at her and proceed.

Examiner: Dr. Pan, please present your findings.

Dr. Pan:
Puan Rahimah’s head is rotated to the right. She has right eye ptosis. There is no strabismus at rest. Both her pupils are spared. There is no fatigability. There is mild impairment of upwards and upwards lateral movements of the right eye. Intorsion is intact. She has diplopia upon looking at all direction except looking downwards . The outer image disappears upon closing the right eye. There is no nystagmus. The rest of the cranial nerves are intact.

I would like to complete my examination by examining the patient’s BP (H/T), urine for sugar (DM), upper limbs and lower limbs for any pyramidal signs including the reflexes (CPEO, ELS) and cerebellar sign. I would also like to look into the fundus to look for any papilloedema. (/retinitis pigmentosa)

PANIC!!!!!??????? Dx????

In summary, Puan Rahimah has complex diplopia and I would like to consider differential diagnosis of

1) Mononeuritis multiplex
2) MG ( no fatigability)
3) Miller Fisher
4) CPEO, Ocular muscular dystrophy

5) Grave’s ( proptosis?)
6) Cavernous sinus thrombosis/ superior orbital fissure syndrome( if V CN is involved)

Examiner: What other investigation would you like to do?

Dr. Pan:
1) ESR to screen for vasculitis
2) MRI of the brain ( infarct / SOL esp at the midbrain)

Causes of isolated III CN palsy
Medical:
1) DM/ H/T/ Vasculitis
2) Multiple sclerosis

Surgical
1) Posterior communicating artery aneurysm/ Midbrain tu
2) Subacute meningitis

Causes of isolated VI CN palsy ( look for involvement of VII CN)
1) SOL
2) DM/ H/T/ Vasculitis
3) Multiple sclerosis
4) Subacute meningitis

Pustular Psoriasis

2007-03-16T19:12:00.000+08:00

Stem
"This young man presented with this condition after being given some treatment for a his plaque psoriasis . Please examine his skin"

Suggested presentation
This febirle unwell-looking young man has generalised widespread creamy white pustules with an erythematous base. Some of the pustules have erupted, resulting in red oozing erosions . The palms and soles are also involved. He also has generalised onycholysis with discolouration and misshaped toes and fingernails.The patient has tenderness and warmth over both knee joints.

The diagnosis is pustular psoriasis complicated by gout. The likely cause for this presentation is massive intradermal steriod injection.

(Patient in this picture had pre-existing plaque psoriasis, so did his father and paternal grandfather. He was given Intradermal methylprednisolone 200mg daily instead of the recommended 10mg per month. Not shown inthe pictres, he had evidence of plaques on his elbows, hairlines and behind the ears)

Questions that may be asked
1. What differentiates this from skin infections?
The pustules are sterile on culture and the patient's white cell count may be normal

2. What is explanation for the patient's knee pain?
Psoriasis is a condition where there is increased cell turnover so there is hyperuricaemia, which results in crystal deposition in knee joins, giving rise to gout.

3, How would you manage this patient?
The patient should be managed like a exfoliative erythrodermic patient, paying close attention to barrier nursing, fluid replacement, prompt treatment of infections, adequate nutrition

4. Name me the definitive treatment for pustular psoriasis.
Acitretin, an oral retinoid.

Contributed by Giant Eagle

Ptosis Revisited

2007-03-13T18:44:00.000+08:00

eMRCPian has done a great job describing ptosis in the April posting. I'm trying my best to further describe all the important causes of ptosis.

En. Ramli, 30 year old gentleman was told by his friends that he has abnormal eyes. Please examine the eyes.

What’s the Dx?

PTOSIS

*An unequal bilateral ptosis could be easily mistaken to be a unilateral ptosis.

Inspect

Dystrophia myotonica look ( suspect during hand shake)
Eye looking downward and outward

Look at the pupils

-dilated in surgical 3rd nerve palsy
i. isolated: PCOM aneurysm( check hemiplegia, cerebellar, extrapyramidal signs)
ii. III, IV, V1, VI CN–superior orbital fissure synd( II involved)/cavernous sinus thrombosis

-constricted in Horner's syndrome (common: Pancoast tu, LMS)
i. V, IX, X ( LMS)
ii. Neck ( inspect for scars, thyroid; palpate for LN; auscultate for carotid aneurysm
iii. Percuss Upper zone- Pancoast
iv. UL - small muscle wasting, pronator drift ( MS, syringomyelia)
sensation
cerebellar

-normal size pupil in MG, CPEO, dystrophy myotonica, Miller Fisher, medical 3rd nerve( DM, H/T, vasculitis)
i. Eyes
1. Fatigability- upward gaze
2. VARIABLE Strabismus and diplopia in MG( no particular CN opthalmoplegia).
Medical 3rd nerve palsy?

ii. Face
1. V CN
2. VII CN
3. Bulbar ( count 1-50)

iii. Muscle
1. Neck Flexion
2. Proximal myopathy
3. Reflex ( ELS, Miller Fisher)

Look for
1) Treatment given: median sternotomy , subclavian line
2) Complication: tracheostomy, gastrostomy
3) Fundus ( CPEO)
4) Ass A/I dis

Ix for MG:
FVC, Edrophonium test, Anti Acetylcholine receptor Ab, EMG, CXR, CT mediastinum

Tx:
Long acting cholinesterase inhibitor
Thymectomy

I Can't Hear Any Heart Sounds!

2007-01-26T00:44:00.000+08:00

Well, based on this opening title alone, if you are the candidate doing station 3 (cardiovascular) and you are stuck with this initial finding, what would you do next?

I attended a UK PACES course last year and this was one of the cases. We (in a group of 7) were instructed to auscultate the precordium of this patient by turns. I practically couldn't hear anything on the left! I immediately moved my stethoscope to the right. The patient smiled at me and said: "You're fast to pick this up. You'll pass." This indeed was a boost to my confidence during the real exam! ;)

The unifying diagnosis I would like to consider for this patient is Kartegener syndrome. My principle findings on cardiovascular examination is that she has dextrocardia. The apex beat is at the right 5th intercostal space. There is no murmur to suggest an intracardiac shunt. Clinically, she is not in cardiac failure and she is in sinus rhythm.

She has obvious finger clubbing and on auscultation of her chest, there are coarse crepitations at the bases which diminish following a cough. I would be keen to examine the abdomen to look for associated situs inversus.

Q: How would you like to investigate this patient?

A: I would do a plain chest radiograph to confirm dextrocardia and to look for features of bronchiectasis.

(Examiner:"Here you are.")

A: The cardiac silhouette falls on the right side and there are ample findings which are in keeping with bronchiectasis. There are cystic changes resembling a bunch of grapes on the lower zones. Tramline opacities are noted especially on the left base. However, the gastric bubble appears to be on the left side hence I think this patient doesn't have situs inversus to complete the syndrome.

Some Drills On Station 5 (Part 2)

2007-01-24T14:23:00.000+08:00

Stem: Look at this patient and proceed.

Suggested presentation:

I would be very much interested in knowing his blood pressure and I would complete my examination by examining the visual field and dipstick his urine for glycosuria.
(Examiner: "His blood pressure is 110/80mmHg and there is no visual field abnormalities")

This patient has acromegaly as suggested by his coarse facies and spade-like fingers. There are prominent supraorbital ridges and the nose and mouth are both relatively big with evidence of overbiting of the lower jaw. On inspection of his oral cavity, there is macroglossia with interdental separation. Tinel's sign is negative. There is no axillary skin tags and excessive sweating. Coupled with a normal blood pressure and normal visual field, I think the disease activity is currently quiscent.

NB: As demonstrated in this case, candidates should not be taken aback by information offered by the examiners midway during your presentation. Instead, you should be keen to expect responses from examiners since that information is important in formulating the complete diagnosis.

Some Drills On Station 5 (Part 1)

2007-01-17T10:29:00.000+08:00

More often than not, candidates would go into a sudden lapse of thought block when they are presented a patient at station 5. Knowing that you'd need to come up with a diagnosis in a very short time, the adrenaline surge and tachycardia invariably complicate the whole picture!

The only way to secure a good chance of passing station 5 is to do a lot a lot a lot of cases.

Since station 5 is a spot diagnosis station. As mention by eMRCPian before, the 'hit-hard' strategy is the strategy of choice. Even though you do not want to commit yourself to a diagnosis, you must be able to come up with a reasonable differential diagnoses within the 1st minute of presentation!

Let's ride!

Stem: Look at this patient's face and tell me what you think.

To Station 4 With Love And Sweats!

2007-01-06T22:44:00.000+08:00

Being one of the most fearsome stations of all, the scenario outlined could well be quite tricky and taunting, nonetheless on the other hand, could be quite straight-forward at times. It is for this very reason it's been said to be the most unpredictable station.

Allow me to share some of the points that I've learnt throughout the journey in becoming an mrcpian;)

Remember these 5 core principles in medical ethics:

Non-maleficence - ie to do no-harm first!
Remember this principle first. You will find that it's applicable in any scenarios, and it's indeed very true in our daily clinical practice.
Beneficence - ie to do good for patients
Patient's autonomy and right to confidentiality
Truth-telling
Justice and sharing - ie fairness in provision of care in face of limited resources

Hence, after spending 14 mins with the surrogate and 1 min of reflection, time for heads-up and face the music! Place your discussion with the examiners based on all these core principles. You won't go wrong. But to get a 4 would require much of your soft skills in tackling the surrogate's emotion and responses.

Here are some illustrations:

A patient with advance statement for no-CPR came in with an umcomplicated MI. Your task is to explain with regards to his advance statement and its application to his current diagnosis.
Principles: Autonomy vs beneficence
Relatives of a patient with poor outlook came to you requesting ICU admission. Your ICU has 1 bed left. A young man with polytrauma is on his way to the hospital. Your task is to address this issue with the relatives.
Principles: Autonomy (any advance statement?) vs justice and sharing of care
You accidentally prescribed bactrim to a patient with a previous history of sulfur allergy. The patient developed Steven-Johnson syndrome. The father is keen to meet you for an explanation.
Principles: Non-maleficence & truth-telling (apology)
A young man is tested positive for HIV. He refused to tell his wife despite adequate explanation. Your task is to meet him and explain with regards to the risk of transmission of HIV to his sexual partner(s).
Principles: Autonomy (confidentiality) vs non-maleficence (public interests) and justice

A Fresh 'n Cool New Year Ahead!

2006-12-31T21:51:00.000+08:00

To all MRCPians and aspiring wannabes out there,

Happy New Year 2007!!

I have the utmost honour to 'inherit' this blog from eMRCPian. Would like to take this opportunity to wish him all the best once again for his wedding and honeymooning :)

Congratulation!

2006-12-18T21:59:00.000+08:00

It had been about 1 year I started this blog. I am glad that the associate authors are taking part actively in contributing to this blog. Thank you.

I would like to take this opportunity to congratulate Axonopathic who had passed MRCP recently in November 2006. He promised me that he will try to share his learning experiences in London, UK.

Let's congratulate Axonopathic for the success of being a member of royal college and also being the 2nd chief author of our blog!

Skin: Hyperpigmentation

2006-12-09T16:02:00.000+08:00

Possiblity of opening statments
Look this lady who presented with weakness, loss of appetite and weight loss.

Suggested examination method
Hands-look at palmar creases for hyperpigmentation (Compare with your own palm)
Mouth-look at tongue, buccal mucosa for hyperpigmentation
Elbow: pressure points hyperpigmentation
Other sites: nipples, previous scars
Look for vitiligo

Tell examiner you would like to complete examination by:
checking her blood pressure (postural hypotension)
look for sparse axillary and puvic hair
Abdomen-?scars of previous bilateral adrenalectomy
Ask to check for visual field defect if you suspect Nelson's Syndrome.

Remember Nelson's syndrome is a enlarging pituitary tumour caused by previous bilateral adrenalectomy (done in the past for treatment of Cushing's Disease. Hyperpigmentation caused by high ACTH levels.)

Suggested presentation
"This young lady has generalized hyperpigmentation, which is more marked in the tongue and the palmar creases. The history suggest that she has Addison's disease. "

Questions you may be asked
(1) What are the causes of Addison's disease?
Idiopathic (80%)
TB (important to remember if you are taking exam in Singapore/Malaysia)
Metastasis
HIV infection

(2) How will you investigate this patient?
Biochemical tests to look for hypoNa, hyperK, metabolic acidosis
Blood glucose to look for hypoglycemia
I will do a screening test using the synacthen test to confirm the diagnosis.
I will also measure ACTH levels and cortisol levels.

Suggested reading for this topic
Polyglandular syndrome type I and II
Interpreting the synacthen tests.

Contributed by Lee Jun @ Giant Eagle @ Suikotsu (Sleeping Bone)

References:
250 cases in clinical medicine by Baliga
An Aid to the MRCP PACES by Ryder

Paget's Disease

2006-11-23T22:35:00.000+08:00

My diagnosis is that this elderly lady has Paget’s disease as evidence by enlargement of the skull, bowing of the Right tibia which is warmer than the left one. She also has a hearing aid which suggests her condition is complicated by deafness. She is kyphotic.

I would like to look at the fundus for optic atrophy and angioid streaks, examining the CVS for heart failure. I would also do a urinalysis for evidence of hematuria (urolithiasis).

Investigations include ALP, urinary hydroxyproline which are elevated and a normal Ca and PO4.

**When is biphosphonates indicated for Paget's ds?

posted by Wuchereria

Marfan Syndrome

2006-11-01T18:49:00.000+08:00

A popular spot diagnosis in MRCP station 5 or may be in CVS station. You notice this man has long fingers ( arachnodactyly).Demonstrate to examiners and convince them that the patient's fingers are long and joints are hypermobile by demonstrating thumb sign ( ask patient to clench her thumb in her fist, the thumb should not exceed the ulnar side of the hand in normal subjects)

Then, look for other signs to suggest Marfan syndrome such as high arched palate ( in this patient), upwards subluxation of the lens, kyphoscoliosis, and chest wall deformity i.e. pectus excavatum.

For the heart, remember you are likely to find either aortic regurgitation or mitral regurgitation.

You Can Do It!

2006-10-16T21:38:00.000+08:00

Dear all MRCPian, the next PACES is coming up.
For those who are going to sit for their MRCP PACES soon, I hope all the best and good luck to all of you.

I always believe that

Where there is a will, there is a way!

Warm regards,

eMRCPian

Lipodystrophy

2006-10-09T19:22:00.000+08:00

Opening Statement
"This 17 year old girl presented to endocrine clinic with a history of polyuria and polydypsia. Please look at her and proceed."

This young girl who is short for her age has masculine facial appearance caused by loss of fat in the face. She has prominent muscles and inframazillary dimples.She also has loss of fat (fat atrophy) in the arms and hands, giving her a muscular appearance.

The diagnosis is partial lipodystrophy.

As the opening statement says she has polyuria and polydyspia, I would like to do a urine dipstick for sugar as this condition is associated with diabetes

Questions you may be asked
(1) What other conditions may be associated with lipodystrophy apart from diabetes
**HIV on antiretroviral therapy
**Mesangiocapillary glomerulonephritis
**Localized scleorderma
**Morphea
**Chronic replasing panniculitis

Contributed by Giant Eagle

Psoriasis With Axial Arthropathy

2006-09-29T18:21:00.000+08:00

Well dermacated erythematous plaque with silvery scales.
I had been quite busy for the past few weeks as I just joined skin department and there are a lot of new things to learn. It is a whole new world for me to explore.

As we all know, the prevalence of psoriasis is about 2% of the population. It is the bread & butter of dermatology practice. Here is one of the new cases that presented with difficulty in extending his neck for the past few years. We nearly miss this sign until he stood up to thank us after the consultation - he is unable to extend his neck to look at us. In addition, he needs to turn the whole body to look to either side.

As the picture shown, the occiput is not able to make contact with the wall when heel and the back are against the wall. It indicates upper thoracic and cervical limitation.

Questions:
1. What are the types of psoriatic arthropathy?
* Arthritis of DIP (Classical)
* RA like arthritis
* AS like arthritis (spondylitis and sacroiliitis)
* Mono- and asymmetrical oligoarthritis
* Arthritis mutilans

2. What is the most common psoriatic arthropathy?
* Mono- and asymmetrical oligoarthritis

Wallenberg's Syndrome

2006-09-14T19:43:00.000+08:00

This Malay gentleman presented with 2 days history of dizziness. He cannot walk steadily without assistance.

Examination of the LL shows hemisensory loss up to neck region over RIGHT side. The muscle power is preserved. The propioception is intact. He is ataxic and there is tendency to fall to LEFT side. The heel shin test is impaired over LEFT side.

Further examination shows LEFT facial numbness with intact corneal reflex. There is signs consistent with LEFT Horner's syndrome i.e. partial ptosis and constricted pupil. The 9th and 10th CNs are intact. The eye movement is normal and there is no diplopia.

He has a LEFT lateral medullary syndrome.

Questions:
1. Where is the lesion?

2. What are the other clinical features?

Turner's Syndrome

2006-09-10T21:02:00.000+08:00

Case record by Wucheceria

Short stature
Webbed neck and low set hairline
Wide carrying angle

Approach

Short stature

Hands
*Short 4th metacarpal
*Wide carrying angle (cubitus valgus)

Face
*Hypertelorism
*Epicanthic fold
*High arched palate

Neck
*Webbed neck
*Low hairline

Chest
*ASD scar
*Shield like chest
*Wide spaced nipple

Lymphoedema
Mental retardation is rare
Left sided heart lesions i.e. aortic stenosis , coarctation of aorta

Questions:
What renal abnormalities are associated with Turner’s
Horseshoe kidney and hydronephrosis

Is pregnancy possible ?
Yes in the mosaic individuals with normal 46 XX cell line

How would you manage such patients ?
Tretment is supportive and includes hormone replacement therapy on attaining puberty, primarily to prevent osteoporosis and induce sexual maturation or menses

Differential diagnosis
Noonan’s syndrome

Some Pics Of Hansen's Disease

2006-09-03T10:22:00.000+08:00

It is still not uncommon to see leprosy patient in Malaysia although we had achieved the WHO "elimination" level i.e. prevalence rate of less than 1 case per 10,000 inhabitants.

Here are some pictures of lepromatous leprosy patient from Sarawak. - courtesy of Giant Eagle.

"Leonine" facies with loss of eyebrow.

Trophic skin changes with ulceration over feet

Close up view over feet

Burn out leprosy with hand deformities

Dermatomyositis

2006-09-03T09:44:00.000+08:00

This lady has dermatomyositis. She has a heliotrope rash over the knuckles (GOTTRON"S Papules), back of the hands, eyelids and periorbital area. She also has nail fold telangiectasia.

(Look also in elbows and knees for Gottron's papules, it may be the only clue you have)

She also has Cushiongoid features, likely due to steroid treatment. (Mention other complications of steroid treatment if any-Cataract, vertebrae fracture, obesity).

There is also proximal muscle weakness and tenderness and the patient has had a muscle biopsy done (look for scars on thigh/upper arm)

Functionally, she has impaired swallowing as she requires a Nasogastric tube

NB Candidates often mispronouce "Gottron's" as "Grotton's". Be careful! Look for other things such as Raynauds, SLE

Questions that could be asked

1. How would you manage this patient?

**I would like to confirm my diagnosis of dermatomyositis by doing the appropriate investigations (eg muscle biopsy, Electromyelogram)

**As this lady is over 40, I would also investigate for underlying malignancy (mention NPC, breast, ovary, Lung and GIT) I would also investigate for connective tissue diseases.

**I will also start patient on high dose steroids and add on steroid sparing drugs.This patient also needs nutritional support as she is cachetic and has dysphagia caused by the disease.(Hopefully by the time you reach this station, your time is up)

2. How to differentiate this rash from SLE rash?

**In SLE, the rash spares the knuckles, and involves the phalanges.

3. How would you classify polymyositis-dermatomyositi?

**I Primary idiopathic polymyositis

**II Primary idiopathic dermatomyositis

**III Dermatomyositis (Or polymyositis) with neoplasm

**IV Childhood dermatomyositis

**V polymyositis/dermatomyositis with collagen vascular disease

The above case and photos are contributed by Giant Eagle

Cushing's Syndrome

2006-08-24T21:29:00.000+08:00

I would be keen to examine this lady's blood pressure and dipstick the urine for evidence of overt glycosuria and proteinuria. I also would like to complete my examination by checking the visual fields and performing a funduscopy to look for evidence of retinopathy and papilloedema. A history of steroid usage is of prudent importance in this patient.

This lady has Cushing's syndrome as evidenced by the presence of moon-face associated with hirsutism and acne. There are buffalo hump and truncal obesity as well. There is thinning of the skin with localised bruises especially over the cubital fossae of both arms. However there is no purplish striae noted on the abdomen and inner thighs. There is no oral thrush. Patient has proximal weakness. The back is straight with no features of kyphoscoliosis.

Questions:
1. What are the causes of Cushing's syndrome?
Outline: Pituitary-driven, adrenal and ectopic or iatrogenic sources.

2. How would you investigate to determine the cause?

I would screen the patient by doing a 24hr urinary free cortisol first and overnight dexamethasone suppression test. A high dose dexamethasone suppression test is then needed to localise the source of excess cortisol. An elevated ACTH level would isolate the source to either from pituitary or ectopic source.

3. What are the other tests to determine the source of ACTH (to distinguish primary from ectopic)?

CRH and inferior petrosal sinus sampling. An MR of the pituitary gland is helpful as well.

4. How would you manage Cushing's syndrome?

Outline: If possible, the underlying source of excess cortisol should be removed. In cases where the source cannot be removed, I would manage the complications which may arise from Cushing's syndrome.

5. What is Nelson's syndrome?

(A reminder: In real exam situation, you are unlikely to get so far. If you do, then there are 2 extreme possibilities, ie, either you score tremendously..or you failed badly!)

The bell has already rang! The answer is in the book :)

Midline Sternotomy Scar

2006-08-23T21:29:00.000+08:00

Case record by Wuchereria

Examine the Cardiovascular system

This pt has a pulse rate of 80/min which is irregularly irregular. There is no radio-radial delay or collapsing pulse. There is no clubbing or peripheral stigmata of infective endocarditis. She is pale. There is no jaundice, cyanosis. JVP is not elevated and there is no pedal oedema of the legs.

On examination of the precordium, there is a midline sternotomy scar.

Apex beat is displaced, 5th intercostals space 2 cm lateral to MCL. No parasternal heave or thrills.

Metallic click of the 1st HS, normal 2nd HS

Lungs clear

I would like to complete my examination by checking the fundus for Roth spot or fundal haemorrhage, look for signs of overwarfarinization, examine the CNS for evidence of CVA, look for splenomegaly, urine dipstick for haematuria, check BP, all peripheral pulses

My diagnosis is that this pt has Mitral valve replacement and is in atrial fibrillation and is anaemic. There are no signs to suggest infective endocarditis, pulmonary hypertension, overwarfarinization or heart failure. There is also no evidence of valve leakage.

Questions:

1. What are the causes of anaemia ?
*Bleeding due to anticoagulation
*Haemolysis
*Secondary to IE

2. Advantages of Porcine heart valve
*No need anticoagulation

3. Disadvantage of Porcine heart valve
*Degeneration with time – may need reoperation (after about 7 years)
*Calcification

Hansen's Disease

2006-08-16T22:14:00.000+08:00

What is your diagnosis if this case appear in skin substation? It is not JVP nor Corrigan's sign! It is a thicken great auricular nerve.

Think of Hansen's disease (Leprosy) in this case. You may see this case in Malaysia PACES center.

The next step is to search for a skin lesion with sensory loss. Ask for contact history

Hypopigmented macules in confluence (patches) of tuberculoid leprosy.

"Leonine facies" of diffuse lepromatous leprosy.

Wasting Of The Small Muscles Of The Hands

2006-08-07T12:54:00.000+08:00

Examination of hands is very common in PACES setting. You may encounter the hands in locomotor substation or neurology station. There are not many differentials that you need to memorize but you need to have a mind mapping about the approach especially in neurology station.
Related post about PACES hands....

1 st case is a 40 years old man with insidious distal weakness for > 12 years. 3 out of his 8 siblings are affected. He has wasting of small muscles of the hands resulting in guttering of the dorsum of the hands. There is generalized areflexia and glove pattern of sensory loss. He came for nerve conduction test which show reduced conduction velocity. The diagnosis is Charcot-Marie-Tooth disease.

2nd case is a middle aged man who had progressive weakness of hands for 10 months. He has wasting and weakness of small muscles of the hands. The hypothenar and thenar eminences are wasted with left more severe than right. There is fasciculation seen and the reflexes are brisk. The sensation is normal. MRI cervical spine and NCS are normal. The diagnosis is motor neuron disease (MND).

3rd case is a 30-year-old lady with a syringomyela developed painless ulcers of the palms and fingers. Other possible skin signs are edema and hyperhydrosis due to interruption of central autonomic pathways.

Confuse? Don't get panic. Just remember several points:
1. We should localize the lesion as LMN i.e. the lesion is at C8-T1 level including the cord, anterior horn cell, nerve roots and peripheral nerves.
2. NMJ is not included because it does not cause wasting. Muscular disorder is not included because it does not usually cause distal weakness.
3. Sensory examination is VERY important in localizing the lesion. For example, if there is sensory loss then MND is excluded from your differential lists.

Please click on the chart for larger figure.

Tunnel for PACES?!

2006-08-06T22:22:00.000+08:00

Where is the tunnel for PACES? Of course, it is not along the PLUS highway in Malaysia!

Here is a lady who came for nerve conduction study. She experience Right hand numbness that disturb her sleep.

Compare the thenar eminence of the Right hand with that of the Left hand and note that it is not as prominent on the Left. It is wasted. This is the result of median nerve entrapment at the flexor retinaculum, leading to carpal tunnel syndrome.

There is weakness of flexion, abduction and opposition of the Right thumb. The sensation also reduced over the lateral three and half fingers.

Then, proceed to elicit Tinel's sign which is positive in this case.

A positive Tinel’s sign for suspected carpal tunnel syndrome results in distribution of paresthesias (shaded area).

1. What is Phalen's maneuver?
2. What is the causes for carpal tunnel syndrome?

Peripheral Neuropathy

2006-08-02T22:43:00.000+08:00

Here is an Indian gentleman who complaints of feeling shaky on walking for the past 3 years. The onset is insidious and his condition gradually worsen for the period mentioned.

There is trophic changes noted over the lower limbs i.e. the skin is shinny, smooth and loss of hair. There is hyperpigmented skin lesions suggestive of diabetic dermopathy. There is no muscle wasting and the power is normal.
There is impairment of sensation to vibration sense, joint position and pinprick over a stocking distribution ( from foot up to knee level). The reflexes are absent.

There is sensory ataxia as evidenced by positive Romberg's sign and stamping gait (broad based gait, foot stamping on the floor)

In conclusion, he has a peripheral neuropathy predominantly involving the sensory component. Functionally, he has sensory ataxia due to impaired joint position sense. The likely cause would be diabetes mellitus in view of the diabetic dermopathy.

I would like to complete my examination by:
1. Checking the upper limbs (sensory loss over a glove distribution)
2. Palpating the peripheral pulses (peripheral arterial disease due to the trophic skin changes)
3. Examine the fundus for diabetic retinopathy.
4. Checking the urine for sugar.

What are the other causes for sensory peripheral neuropathy?

IE signs

2006-07-30T23:15:00.000+08:00

OK, enough neurology cases for July. I will show you some classical signs of infective endocarditis.

SPLINCTER HAEMORRHAGE

subungual linear “vasculitic” lesions

OSLER’S NODES

red, raised tender nodules on the pulp of the fingers (or toes), or on the thenar or hypothenar eminences

ROTH’S SPOT

intraretinal haemorrhages with white centers representing fibrin thrombus occluding a rupture blood vessel

JANEWAY’S LESION

Non-tender, erythematous maculopapular lesions, containing bacteria, which occur very rarely on the palms and pulps of the fingers

CLUBBING

Brown Sequard Syndrome

2006-07-23T23:19:00.000+08:00

I am now working in neurology unit. Hence, I will be showing you all more neurology cases. Recently, I came across a case of SLE who presented to us with subacute onset of right LL weakness. Clinically, she has monoparesis of right leg with reduced tone, the reflexes are reduced and extensor plantar response. There is loss of joint position and vibration senses on the right side. There is loss of pain senses on the left side up to the level of T7.

These features suggest a diagnosis of right hemisection of the spinal cord. An urgent MRI of spine is warranted to exclude space occupying lesion like abscess or tumour.

Our working diagnosis is tranverse myelitis related to SLE.
The diffential diagnosis would include tumor (primary or metastatic), disk herniation, herniation of the spinal cord through a dural defect, epidural hematoma and vertebral artery dissection.

More about Charles-Édouard Brown-Séquard .

Proximal myopathy

2006-07-13T18:49:00.000+08:00

The clinical diagnosis of proximal myopathy is usually straightforward. Proximal muscle wasting and weakness is easily demonstratable.

Tips:
**The weakness is bilateral and usually symmetrical.
**The sensory is always INTACT!

The causes that you need to consider are:
1. Muscular dystrophy
**Duchenne/ Becker muscular dystrophy (look for pseudohypertrophy of calf muscle
** Fascioscapulohumeral dystrophy (look for facial muscle weakness)
**Limb girdle muscular dystrophy

2. Inflammatory muscle disease
** Polymyositis (muscle may be tender)
** Dermatomyositis (Facial heliotrope rash and Gottron's sign)

3. Endocrinopathy
** Cushing's syndrome
** Thyrotoxicosis
** Acromegaly
**ALL will have obvious external features

4. Metabolic myopathies
** Hypo/hyperkalemia, Hypo/hypercalcemia

Wasting of deltoid muscle
Difficulty in standing up from squatting

This patient was referred to neurology clinic for an investigation. He was then planned for an elective procedure.

What is the respective investigation and procedure?

Tips for Fundoscopy

2006-07-04T18:32:00.000+08:00

One of the tough station in PACES as you need to complete your examination within 3 mins ( another 2 mins for discussion). If you are unlucky, you might need to examine via a small pupil (normally last candidate of the day).

There are several tips to get the correct diagnosis:

1. Prepare the patient by giving a clear instruction. Here is my suggestion.

Mr. X, I am going to come near you and examine your R/L eye with this light. It might be uncomfortable. Please bear with me. Now, look straight and keep your eyes still. Don't move your eyes but you can blink as you wish.

2. Always check the macula area before presenting your findings.
Mr. X, please look into my light now.
3. Think of 3 main diagnosis you need to know for PACES

Diabetic eye, retinitis pigmentosa, optic atrophy.

Good luck!

The Journey for MRCPian

2006-06-27T22:55:00.000+08:00

This is my advice for every inspiring MRCPian. Start practicing now and take every single opportunity to present to your seniors, collegues or even house officers! Every effort you made brings you closer to get your MRCP!

Pes Cavus

2006-06-26T18:51:00.000+08:00

Pes cavus or high arched foot is an important sign for PACES candidates. It carries a lot of weight in neurology station.

1) It means the underlying cause is long standing.
2) It means you need to strongly consider these diagnosis:
** Charcot-Marie-Tooth ds
** Friedreich ataxia
** Syringomyelia
** Others: poliomyelitis, cerebral palsy