Medicine for MRCP & Medical Students

MCQ for medical students and MRCP Part 1 or 2a

2012-02-14T19:22:00.000-08:00

A 73 years old Chinese lady came to you in the outpatient complaining of chronic pain over the joints of the hands. All the following are true except :

A. the knees and the cervical region may have similar problem

B. the first line of pain relief medication is paracetamol

C. Leflunamide is one of the treatment as a DMARDs

D. The PIP involvement is called Bouchard's nodes

E. The DIP involvement is called Herberden's nodes

Practical Neurology by Jose Biller

2012-02-10T15:56:00.000-08:00

Medical Students,Residents and Fellows in Internal Medicine or Neurology of USA...... good news, this great book ......It will also be useful for USMEL and the RITE exam !

if you are interested in the above book, please email me at thienthienlim@gmail.com

Cost of the book : US$85.00

Shipping : Free (only to USA)

Condition : Brand new with plastic cover not opened

MCQ for Medical Student

2012-02-06T19:06:00.000-08:00

The following are causes of the above except :

a. Cyclosporin

b. Phenytoin

c. Thiazide diuretic

d. Vit C deficiency

e. acute myeloid leukemia

MCQ for MRCP part 1 and 2a

2012-02-05T11:11:00.000-08:00

This gentleman arrived in the ER with shortness of breath and difficulty in swallowing.

Question 1 :

What is the pathophysiology of his problem ?

a. Antibodies to presynaptic P/Q type voltage gated Ca channel

b. Antibodies to voltage gated K+ channel

c. Antibodies to postsynaptic Ach receptor

d. Antibodies to voltage gated Na channel

e. Antibodies to presynaptic Ach receptor

After assessment of airway, breathing and circulation, the patient was intubated/stabilized and was admitted to the ICU.

What is the treatment of choice for this patient ?

a. IV immunoglobulin

b. IV cyclophosphamide

c. 3,4-aminopyridine

d. conservative management

e. I don't know the answer, refer to the neurology experts !

5th MRCP PACES Preparatory course PENANG

2012-01-25T07:52:00.000-08:00

MRCP PACES MOCK EXAM 2012

2012-01-20T04:35:00.000-08:00

Hospital Batu Pahat will be organising an MRCP PACES MOCK EXAM 2012 on 10/3/2012. Examiners include Dr Christopher Lee, Dato Dr Sree Raman, Prof Dato Raymond Azman Ali, Datuk Aziah(IPR), Dr Hooi Lai Siong, Dr Lee Man Pin, Dr Paras Doshi, Dr Kauthamon as our distinguished examiners.

For more information, please email: md_richardchee@hotmail.com

2012-01-15T14:50:00.000-08:00

This 18 years old boy has complaints of releasing his grip when intending to throw a ball.

What is the diagnosis ?

Good news for overseas medical students & MRCP candidates !

2011-10-28T18:01:00.000-07:00

CLICK HERE FOR SAMPLE OF BOOK

Now you can buy the PACING THE PACES book at a sale price of

US$30 + postage(depending of country) +4.5%(for paypal)

and pay securely via paypal.

If interested, pls email thienthienlim@gmail.com

http://www.scribd.com/fullscreen/70723450?access_key=key-1xcbp2quv4cs0mk464id

Quiz for medical students and MRCP candidates

2011-10-07T11:02:00.000-07:00

Question 1

What is shown in the picture above ?

Question 2

What other signs would you look for ?

Question 3

What would you ask in the history ?

Question 4

What is important in the family history ?

Question 5

What is the diagnostic criteria ?

Question 6

Which gene is responsible for this ?

Neuroimaging quiz

2011-08-10T14:50:00.000-07:00

This 45 years old man presented with a complex partial seizure. What does the MRI scan show and what is the diagnosis ?

MRCP PACES reader !

2011-07-17T12:44:00.000-07:00

Dear MRCP/Medical Student readers of this blog,

Thank you for following this blog. It is dedicated to all of you. The short case examination can cause you to have tachycardia during the examination and can also be fun if you have prepared well for it. It is a game and to see how well you play it.......

This year, I have got good news and not so good news. I will start with the not so good news. The not so good news is that I would not be able to organize the 5th MRCP Preparatory Course in Penang this year. I am not sure if anyone else is organizing it.

The good news is that I have compiled the cases in pictorial format into 2 books

1) PACING THE PACES - More than 300 over pages of diagrams, photos including cases of histories and communication skills. High quality paper and notes which is easy to read.

2) The Medical Short Case : An Examination Guide - More than 200 pages with approach and cases. No history or communication skills chapter in the book.

As the preorder for the book, we are selling the books :

Book 1 - RM50/book (excluding postage)

Book 2 - RM35/book (excluding postage)

Total for 2 books RM85 (excluding postage). If you are interested, please email me at thienthienlim@gmail.com to make orders before the price hike. The price is limited to residents in Malaysia only.

If you have finished reading the books, I am sure you will be able to approach the cases well and it will turn out to be a lot of fun.

Rash

2011-07-01T06:45:00.000-07:00

What is shown in the picture ?

How would you examine this patient ?

Hand Quiz

2011-06-29T06:13:00.000-07:00

This patient presented with epistaxis. Please examine the hands.

What is shown in the picture above ?

What else would you examine ?

What are the associated clinical manifestations ?

What is the diagnosis ?

What is the most likely cause for the epistaxis ?

What are the investigations ?

Outline the management.

Get the latest copy of PACING THE PACES. While stocks last. For more info, please email thienthienlim@gmail.com

The new awaited PACING THE PACES book.......

2011-06-24T06:19:00.000-07:00

This book is created for those taking the final year medical student exam and the MRCP PACES exam. Focus on short cases and also history taking and communication station. Also has experiences of PACES candidates...

A must buy book with lots of algorithms and coloured pictures....

The past 4 years of the Penang MRCP PACES course (2007-2010) and more :)

If interested, pls email me at thienthienlim@gmail.com

Station 4 PACES - Break bad news

2011-04-03T00:21:00.000-07:00

How a Physician should Break Bad News to a Patient

(Adapted from Ptacekm Eberhardt, 1996), AAN Guideline Summary for Clinicians

Location

Quiet , comfortable and private

Structure

In person, face to face
Convenient time
Enough time to ensure no rushing or interruptions
Make eye contact and sit close to patient

Participants

Have patient's support network available

What is said

Find out what the patient already knows about the condition
Ascertain how much the patient wants to know about the disease
Give a warning comment that bad news is coming
Acknowledge and explore patient's reaction and allow for emotional expression
Summarize the discussion verbally, in writing and/or audiotape
Allow for questions

Reassurance

Explain whether the complications of the disease are treatable
Indicate that every attempt will be made to maintain function and patient's decision will be respected
Reassure that care for the patient will continue
Discuss opportunities to participate in research treatment protocols
Acknowledge willingness to get a second opinion if the patient wishes

How it is said

Emotional manner : warmth, caring, empathy, respect
Give news at person's pace; allow patient to dictate what he or she is told

Language

Simple words, yet direct; no euphemisms or medical jargon

Spot diagnosis

2011-04-01T17:29:00.000-07:00

This patient is in Station 3. What is shown and what is in your mind ?

Picture Quiz - Face

2011-03-23T16:17:00.000-07:00

Please state the sign shown in the picture.

List the likely cause of this.

3rd Edition Sarawak Handbook of Medical Emergencies

2011-03-19T19:34:00.000-07:00

The best book ever created for management of medical emergencies !

The new edition promises great updates, coloured pages and better quality paper.

If you are interested, pls email me at thienthienlim@gmail.com.

The book costs RM50/book. (Not applicable for overseaseas)

Free courier service for sending within Malaysia for at least 20 copies.

3rd Advances in Neurology - Dedicated to MRCP PACES candidates

2011-03-06T06:08:00.000-08:00

Clinical Examination

2010-11-15T05:34:00.000-08:00

It has been a while since I wrote. There is nothing more important in short case examination and PACES than to see more and more cases everyday and to practice again and again what you would do in your exam. Neurology is a very interesting field.....

You can see in the video, movements of the left lower limb.....

The question is ..

is this a movement disorder, seizure, a voluntary movement or something else ?

I saw this patient today and thought that many who read this will learn something from this.

(Do not miss this in the exam !)

MRCP PACES book 2nd hand for sale - Book sold on 28/11/10

2010-11-14T07:41:00.000-08:00

MRCP PACES Communication book - the best and easy to read.

There is a second hand one from a friend who wants to sell it at RM60.00 or USD 20 . If interested, pls email me at thienthienlim@gmail.com

All the best in those who will be getting the MRCP PACES results soon....

Stroke syndrome

2010-07-06T05:33:00.000-07:00

Adapted from Neurology Journal

Some said this blog is too simple. Just a challenging one.

Hint : It is a stroke

1) Where is the lesion ?

2) What is the syndrome called ?

PACES

2010-06-10T08:28:00.001-07:00

Meningitis

2010-06-06T04:08:00.001-07:00

MCQ QUESTION !

Which of the following is not part of the empirical treatment of bacterial meningitis

A) IV Ceftriaxone

B) IV Dexamethasone

C) IV Hydrocortisone

D) IV Ampicillin

E) IV Cefotaxime

4th MRCP PACES Preparatory Course 2010 Penang

2010-05-27T03:30:00.001-07:00

APPLICATION FOR PARTICIPATION CLOSED . 3 June 2010.

It has been sometime since I last wrote. It has been a busy year. Neurology is a wonderful field. It makes you grow more grey matter and white hair.

It is the time of the year again. Well, this year a little early because some of us will be going to Kuala Lumpur soon.

This year the course will be in Penang General Hospital, 31 July 2010 to 1 Aug 2010.

Sits are limited !!

Thank you for the quick response. We have exceeded the number of candidates.

The course is confirmed to be only 2 days - On the 31st July 2010 and 1st August 2010

4^th PENANG MRCP PACES COURSE TIMETABLE

VENUE : ACC BUILDING PENANG GENERAL HOSPITAL

Day 1 (Saturday, 31^st July 2010)

	Abd A	Abd B	Resp A	Resp B	CVS A	CVS B	Hx A	Hx B
0800 – 0830		*REGISTRATION*
0830 – 0900		*BRIEFING*
0900 – 0945	1a	1b	2a	2b	3a	3b	4a	4b
0945 – 1030	1b	1a	2b	2a	3b	3a	4b	4a
1030 – 1115	4a	4b	1a	1b	2a	2b	3a	3b
1115 – 1200	4b	4a	1b	1a	2b	2a	3b	3a
1200 – 1230		*BOEHRINGER*	*LUNCH*	*TALK*
1230 – 1330			*LUNCH*
1330 – 1415	3a	3b	4a	4b	1a	1b	2a	2b
1415 – 1500	3b	3a	4b	4a	1b	1a	2b	2a
1500 – 1545	2a	2b	3a	3b	4a	4b	1a	1b
1545 – 1630	2b	2a	3b	3a	4b	4a	1b	1a

Day 2 (Sunday, 1^st August 2010)

	CNS A	CNS B	COMM A	COMM B	St 5 A	St 5 B
0830 – 0930			*LECTURE*	*(PROF*	*RAYMOND)*
0930 – 1030	A1	A2	B1	B2	C1	C2
1030 – 1130	A2	A1	B2	B1	C2	C1
1130 – 1230	C1	C2	A1	A2	B1	B2
1230 – 1330	C2	C1	A2	A1	B2	B1
1330 – 1430			*LUNCH*
1430 – 1530	B1	B2	C1	C2	A1	A2
1530 - 1630	B2	B1	C2	C1	A2	A1
1630 – 1700			*FEEDBACK*

Dermatology Symposium

2010-04-08T18:06:00.000-07:00

Hi !! Guess the picture on top ! If you can't or can, pls attend this symposium :)

Department of Dermatology, Penang General Hospital will organise Penang Dermatology Symposium at Auditorium, Ambulatory Care Center (ACC) Penang General Hospital on 8^th – 9^th May 2010 (Saturday-Sunday).

The symposium is organised in collaboration with PGMES, Hospital Pulau Pinang, Dermatological Society of Malaysia (PDM) and Faculty of Dermatology, Academy of Medicine, Malaysia

Penang Dermatology Symposium is specially dedicated to doctors with special interest in Dermatology. This symposium is opened to all doctors (both government & private).

The aims for this event are to provide a regular continuous medical education (CME) programme in dermatology for practicing practitioners and to provide an update of various topics in dermatology.

Please help us to spread the news to all doctors in your practising hospital and your friends.

Thank You

Regards,

Dr Tan Wooi Chiang

Department of Dermatology

Hospital Pulau Pinang

CONTACT

MA Lim Tong Sun

SN Siti Rafeah

Department of Dermatology

Hospital Pulau Pinang,

Tel: 04-2225250

Fax: 04-2281737

Clubbing

2009-10-06T23:18:00.001-07:00

It's been some while since I last wrote. I have been busy with Neurology. Well, this patient is a 60 years old Malay man who was admitted to my ward with progressive L sided weakness over a week. He is non toxic looking and there is no stigmata of chronic liver disease. He has been a chronic smoker. To tell the truth, I was rather upset that 2 of my house officers could not come to a conclusion even after I mentioned the gross clubbing in this patient.

I hope medical students reading this will practice what has been learned in medical student years.

This is a clear cut case of Ca lung with metastasis to the brain.

What I would like to stress here is - Do not forget the causes of clubbing !

Respiratory :

Ca lung

Pulmonary fibrosis

Bronchiectasis

Chronic suppurative lung diseases

Cystic fibrosis

CVS :

Congenital cyanotic heart disease

Eisenmenger syndrome

Infective endocarditis

GI :

Chronic liver disease (Cirrhosis)

Inflammatory bowel disease

Thyrotoxicosis (pseudoclubbing - acropachy)

Plantar Response - Other than Babinski

2009-06-22T08:34:00.000-07:00

Other than Babinski sign, what other signs do you know ?

In upper motor neuron lesion, the big toe will dorsiflex with the following :

Gordon reflex – On applying pressure to the muscle of the calf

Oppenheim sign – on applying heavy pressure with thumb and index finger to the shin, stroking downwords from below the knee down to the ankle

Bing reflex – when the dorsum of the toe is pricked with a pin

Schaefer reflex – pinching the Achilles tendon sufficiently to cause pain

Chadock reflex – on stroking the lateral side of the foot, beginning below the malleolus and extending anteriorly along the dorsum of the foot to the base of the big toe

Gonda reflex – grasping the small toes between the fingers, slowly and forcibly flexing the toe and then suddenly releasing the toe

I know an MRCP examiner who likes to ask this question. Try practicing it ! Physical examination is the most crucial step in Neurology.

Infectious Disease for MRCP Part 2a

2009-06-06T00:08:00.000-07:00

39 years old 39 years old Malay Man presented with fever for 1 week associated with cough, yellowish sputum, pleuritic chest pain. No haemoptysis, loss of weight or night sweats. Chronic smoker. Also has diarrhoea for 1 week.

Examination reveals clubbing, bibasal crepitations, hepatosplenomegaly. Multiple L/N enlargement.

Hb 10

WBC 4.1

Plt 43

Na 112 K3.2 U 3.8 Cr 69

pH 7.43 pCO2 2.4 pO2 9.8 HCO3 12 BE -10 SpO2 95%

What is your choice of treatment ?

A. IV Ceftazidime 2 g stat and 8H

B. IV (sulfamethoxazole and trimethoprim)Bactrim 3 ampules stat & qid

C. Isoniazid, Rifampicin, Ethambutol and Pyrazinamide

D. IV Acyclovir 500 mg stat and 8H

E. IV Amphotericin B

MRCP PACES Course 2009

2009-05-26T03:59:00.000-07:00

The time we feared most and the time we can't wait for it to be over. However, we choose to face it. PACES exam.....

We know that part of it is due to pure luck but if you are better prepared, the chances of passing is much higher.

Once again, Penang General Hospital, Seberang Jaya Hospital and Penang Medical College is planning for a MRCP PACES course the August 29 and 30. This is a soft launch for the course for those whom I am grateful for keeping up this blog.

Thank you very much for the support. All entries are now closed.

All the best !!

DOWNLOAD REGISTRATION FORM HERE

Neurology Quiz

2009-05-22T17:12:00.000-07:00

(Archieves of Neurology Vol 66 (No 4) Apr 2009

What is the diagnosis and what is the differentials for this ?

Tuberculous meningitis

2009-05-21T08:57:00.000-07:00

A 45 year old man was admitted with a 3 day history of coma following 2 weeks of headache and fever. Examination revealed a GCS of 8/15, neck stiffness, and a complete R oculomotor nerve palsy. Examination of the CSF showed an opening pressure of 20 cmH2O, 800 leucocytes.mm3 (30% neutrophils, 70% lymphocytes), protein 180 mg/dl, CSF/ blood glucose 0.18. Gram and Ziehl-Neelsen stains of the CSF were negative. Culture of the CSF on Lowenstein Jensen media grew Mycobacterium tuberculosis.

(Adapted from Practical Neurology 2002)

This type of scenario can come out in the Part 1 or 2a MRCP and medical student exams. Not possible for PACES.

Name 3 complications of TB meningitis that may need neurosurgical intervention.

Meningitis

2009-05-10T02:27:00.000-07:00

Photo taken form www.thereddragonhood.com/ images/rabbit.jpg

Text adapted from Archieves of Neurology (April 2009)

A 21 years old previously healthy man presented with 7 days cough with black and yellowish sputum, fever, chills, myalgia and pleuritic chest pain. 3 days before admission, had progressive worsening headache with neck stiffness and 8 episodes of watery diarrhoea

He had taken amoxycillin for 1 day

He had recently changed job, working as a professional landscaper 7 days before onset of symptoms

He had performed lawn mowing and leaf blowing services and noted he had dead rabbits in the areas he worked

T - 39.6 C, Alert, orientated to time, place, person

Stiff neck, no weakness or numbness

Lungs - bibasal crepts with exp ronchi

No lymphadenopathy, skin lesions, ulcerations

CT brain - Normal

WBC - 10.4 (78% N) ESR - 40 mm/h

CSF - Cell count 1416/mm3, 19% N 73% L RBC 23, glu 41 mg/dl(glu 123 mg/dl), pro 2660 g/dl

Gm stain CSF -ve

CXR - N

MRI - cerebellar tonsillar herniation consistent with Chiary Type 1 malformation without evidence of brainstem syrinx

Treated with IV Ceftrixone and IV Vancomycin

Day 4 , headache worse and developed diplopia and nausea

Repeated LP -Opening pressure - 49 cmH2O, total nucleated cell count 2590/mm3 32% N 43%L 25% M, glu 28 mg/dL, pro 2950 g/dL (RBS - 128 mg/dL)

Gram stain negative

What is the diagnosis ?

Parkinson Disease

2009-04-27T07:53:00.000-07:00

Picture taken from http://www.goldbamboo.com/pictures-t1604.html

For those taking MRCP PArt 1 Ireland (True of False)

The following increases the risk of Parkinson disease

A. Tea

B. Smoking

C. Coffee

D. Low socioeconomic status

E. Physical inactivity

Excellent Neurology book

2009-04-27T07:31:00.000-07:00

Congratulations to Dr. Eow and Dr. Samuel for coming out with this excellent book with colours and lots of algorithm with facts for the MRCP candidates, medical students and trainees of Neurology. A 393 pages book.

If there is anyone who is interested, feel free to contact me at thienthienlim@gmail.com.

Spinocerebellar Ataxia

2009-04-25T02:19:00.000-07:00

Just a stimulus to all inspired doctors, physicians and neurologists. A very touching video from youtube on spinocerebellar ataxia.

A reminder to those sitting for the next PACES exam. If you see a young man or lady with cerebellar signs and pyramidal signs, always think of

1) Spinocerebellar ataxia

2) Multiple sclerosis - transverse myelitis with cerebellar involvement (classical MS)

3) Friedrich's ataxia

ECG Quiz

2009-04-24T19:43:00.000-07:00

This is a 34 years old man who was admitted with a syncopal attack. ECG shows the above. What is the diagnosis and what would you do next.

This question recently came out in the MRCP PACES exam Part IIa.

Rheumatology/Endocrine quiz

2009-04-11T03:11:00.000-07:00

Would anyone want to comment on these photos which I took of a boy when I was working in Casualty?

Vitiligo

2009-04-10T03:43:00.000-07:00

This patient has areas of depigmentation around the mouth, the upper limb, legs and trunk. He has vilitigo.

Vitiligo affects 1% of the population. Equal between males and females, although more females present to the skin clinic. Family history in 1/3 of patients.

They have Koebner's phenomenon - lesion appearing on the site of lesion.

When you see a patient like this, look for other features of autoimmune

Thyroid disorder - Hashimoto's thyroiditis, Graves' disease

Pallor - Pernicious anaemia

Pigmentation of buccal, skin crease, hypotension - Addison's disease

Tetany, cramps, paraesthesia, Chvostek's and Trousseau's sign - Idiopathic hypoparathyroidism

Fundus - diabetes mellitus

Lungs (fine crepts) - Fibrosing alveolitis

Jaundice - Chronic active hepatitis

Excoriation marks, xanthalesma, pigmentation - primary biliary cirrhosis

rash, arthritis, prox weakness - SLE, RA, dermatomyositis, polymyositis

Look out for polyglandular autoimmune disease

What are the 2 types ?

Skin Quiz

2009-04-07T02:57:00.000-07:00

This gentleman complaints of this rash over the face.

Describe the rash.

What is the most likely cause.

What investigation would you do ?

What one question would you ask this patient ?

What treatment would you give to this patient ?

Pulmonary embolism

2009-03-31T02:00:00.000-07:00

Case by Chye Chung

Thanks for the case which is a good case to discuss.

28 years old Malay man who is in an army, presented with sudden onset of shortness of breath and localised pleuritic chest pain for 1 day. He also has non-productive cough and with an episode of haemoptysis, low grade fever without chills and rigors and rashes. He had previous history of trauma to the knww and ACL repair done 2 months ago. No history of pneumonia, PTB, recent air travel or long journey drive. No other medical illness.

Physical examination was unremarkable and lungs clear with no loud P2

D-dimer 300

Plt 409

PT12.9, aPTT 29.2 INR 1.07

pH7.469, pCO2 72.0, HCO3- 25.8, BE 3.3 O2 sat 95.4%

CXR normal

Would anyone like to comment on the ECG and CTPA ?

Thanks again to Chye Chung for the post !

ECG Quiz

2009-03-29T04:55:00.001-07:00

What abnormality is shown ?

What is the underlying problem ?

What is your management ?

Quiz

2009-03-28T00:05:00.000-07:00

What sign is shown here ?

Where is the lesion ?

What are the possible causes ?

What investigation can you perform ?

Quiz Skin

2009-03-27T07:30:00.000-07:00

What is the diagnosis and why ?

What are the complications ?

What is the treatment ?

Behcet's Disease

2009-03-26T23:53:00.000-07:00

Sourece : www.dermis.net

I saw a patient in the ward today whom my MO told me that she had ulcers in the mouth and genitalia. One of the diagnosis that came to my mind at that time was this. Common in MRCP PACES part 1 and 2a. Not common in PACES MRCP.

What is the diagnosis ?

What test can be done to support the diagnosis ?

What is the diagnostic criteria ?

What is the treatment ?

Hulusi Behcet was born on Feb 20 1889 in Istanbul. As Professor and Director of Department of Dermatology in Istanbul University, he saw the first case of his disease with oral apthous ulcers, genital ulceration, erythema nodosum and visual loss in 1924. The patient was diagnosed as tuberculosis or syphilis, but his diagnosis was viral infection. He died of heart attack on March 8 1948.

Behcet disease is a recurrent systemic inflammatory disorder of unknown aetiology.

It was first described in 1937 as a triad of recurrent oral ulceration, genital ulceration and uveitis.

Males are more common, usually in the 3rd decade.

Associated with HLA B-51

Common in Turkey, Mediterranean and Japan

Diagnostic criteria - International Study Group for Behcet's Disease 1990

Recurrent oral aphthae - at least 3x in a year

PLUS 2 of

Genital ulceration - active lesion/scar
Skin lesion - erythema nodosum, foliculitis, other ulcerations
Eye involvement - anterior or posterior uveitis, or retinal vasculitis
positive pathergy test - skin hyperreativity to pin prick( sterile pustule formed in 24 - 48 hours)

Treatment involves Steroids, cyclosporin, cyclophosphamide or azathioprine.

Colchicine may be effective in treating ulceration.

Superior Vena Cava Obstruction

2009-03-25T07:36:00.000-07:00

I still remembered during my 2nd year as medical student that one of my lecturer who was an Anaesthesiologist(Dr. Murthy) who took us for Respiratory system showed us one case in Sarawak General Hospital.

His words : Look at this patient and remember this forever because you may not see it for a long time to come

He performed the Pemberton sign by asking the patient to lift his arms and immediately, the patient's face became plethoric and his voice became rather hoarse that he had to immediately put down his arms.

You may be asked to examine the respiratory system and you'll find

1) Dilated veins over the chest

2) Plethoric face, occasionally with congested eyes

3) Non-pulsatile raised JVP

4)Pemberton sign positive (you may not want to perform this but offer to the examiner because you may distress the patient which will then cause you to fail)

5) Talk to the patient to notice the hoarseness of voice

You are also expected to find the cause for this which almost always caused by lymph node compression due to malignancy.

The above patient has Non-Hodgkin's lymphoma with SVC obstruction and is in respiratory distress.

Argyll Robertson pupil

2009-03-23T05:36:00.000-07:00

This is an interesting video I downloaded from youtube. I am sure it will be benefeficial for medical students to understand this.

I used to have problem remember when the pupil constricts and when it dilates till I heard this joke :

A prostitute will accomadate but will not react.

So in Argyll Robertson pupil(due to Neurosyphilis), the pupil will constrict to accomadation reflex but will not constrict to light - just as what the video showed.

It is due to damage to the periaqueductal area and is a classic sign.

The pupil is small, irregular and fixed to light but reactive to accomodation

Other causes of what perhaps incorrectly called AG pupils are pinealomas, diabetes, brainstem encephalitis, multiple sclerosis and Wernicke's encephalopathy. These conditions cause fixed semidilated pupils and sometimes unequal pupils; only a small, irregular, fixed pupil should be attributed to neurosyphilis.

I was fortunate, well unfortunate for the patient to have managed a case of neurosyphilis 2 years ago in Neurology . I still remembered the LP I did for the patient (as above) which showed VDRL positive in the LP. Patient actually improved after treated with Penicillin.

Now, the question I want to ask is - what if you get pupils which react to light but not to accomodation (reversed Argyll Robertson pupil). What is the cause ?

Clue : It occured in 1920s

Quiz

2009-03-23T03:56:00.000-07:00

I am sure you know the answer if you are from Malaysia.

What is the diagnosis and what is the classical description ?

Cutaneous T cell lymphoma

2009-03-13T20:32:00.000-07:00

I am sure that this is possibly seen during the MRCP PACES exam. I have managed to see a few of these patients while travelling through the journey in MRCP and I could remember my friend who showed me this while patient was in the skin ward. Unfortunately the patient died a few days later.

So, could anyone tell me what is the diagnosis ?

Cutaneous T-cell lymphoma(CTCL is a form of T cell lymphoma first manifested in the skin, but because the process involves the entire lymphoreticular system, the lymph nodes and internal organs become involved.

Another term - mycosis fungoides (nothing to do with fungus)

Plaques, scaling or non-scaling, large(>3 cm) at superficial

(looks like eczema or psoriasis initially), later it becomes thicker and "infiltrated"

Nodules and tumours with or without ulcer

Poikiloderma with or without plaques and nodules

Extensive infiltration can cause leonine facies

Often spares exposed areas initially

Checklist of diagnosis :

1) History

2) Lymph node - biopsy if palpable

3) Skin biopsy with 1 micrometer sections

4) CXR

5) PBF

6) CT scan abdomen

7) Buffy coat - abnormal circulating T cells (Sezary type) and increased WBC (20,000)

Management :

pre CTCLor proven plaque stage with no lymphadenopathy/criculating T cells - PUVA photochemotherapy in most effective, topical chemotherapy with notrogen mustard in ointment base(10mg%)

If isolated tumours develop, should be treated with local x-ray or electron beam therapy

Extensive plaque stage - electron beam plus chemotherapy

Source :

www.onexamination.com
Color atlas and synopsis of Clinical Dermatology by Thomas B. Fitzpatrick et. al. (McGraw Hill)

Chronic liver disease

2009-03-12T06:49:00.000-07:00

The above picture shows gynaecomastia and multiple spider naevi.

When you see this in the exam whether medical student or MRCP, think of none other than chronic liver disease (liver cirrhosis)

You need to know the signs at your finger tips.

Nails - leuconychia, clubbing

Wrist/Hands - flapping tremor, palmar erythema, Dupuytren's contracture

Face - Jaundice, Parotid swelling(esp alcoholic), look also for KF ring(Wilson)

Chest - Gynaecomastia, spider naevi, loss of axillary hair

Abdomen - Caput medussa, prominent veins, Ascites, Splenomegaly

Legs - Oedema

Note that you rarely get hepatomegaly in chronic liver disease because by then the liver would be cirrhotic and shrink. However, if it is enlarged, think of malignant transformation or alcoholic liver disease.

Can you list the investigations you would perform in these patients ?

Neurology Quiz

2009-02-26T05:16:00.001-08:00

1) Present your findings.

2) What is the diagnosis ?

3) Give reason for your answer.

4) What other differential diagnosis ?

5) What other signs would you look for ?

Ptosis/Exopthalmos

2009-01-29T06:49:00.000-08:00

Can you decide during the PACES MRCP exam whether the R eye is having exopthalmos or the L eye is having ptosis ?
Do you need to toss the coin to decide this in the exam.....50% right, 50% wrong.

If you see the neck you may see a goitre but again...don't be fooled as Graves disease may coexist with myasthenia gravis as both of them are autoimmune disease

One technique to know fast is think logically -
If you see this patient in Station 3(Neuro) - the possibility of L ptosis is higher
If you see this patinet in Station 5(Endocrine) - the possibility of R exopthalmos is higher

So, in Station 3, you would check the eyes as if it was approach to ptosis and if in Station 5 you would check the eyes and look for signs of thyrotoxicosis.

This patient actually has Graves disease.

Giant cell arteritis

2009-01-27T02:26:00.000-08:00

You will hear this term over and over again from medical school to MRCP PArt 1 to MRCP PArt 2a to PACES(most of the time in history station for differential of headache or transient blurring of vision).

Mean age of diagnosis 70 years old
Slightly more common in women

Symptoms :
Headache - usually localised
Jaw claudication (pain on chewing)
General malaise
Proximal muscle stiffness and pain
Visual loss (Amaurosis fugax)

Signs :
Tender and thickened scalp veins
Optic disc swollen and later pale (AION)

Investigations :
ESR elevated (one of the differential for ESR >100)
Raised CRP
Raised ALP
Superficial temporal artery biopsy - intimal thickening and medial damage, giant cells with inflammatory cell infiltration in the internal elastic lamina (GOLD STANDARD)
Management :
A general treatment regime for GCA patients that many physicians follow begins with a 70mg/day prednisone dose.

After the first week, the dose is reduced by 10mg every week until the dosage reaches 20mg/day (Schmidt, 2006).

However, some physicians recommend that the high initial dose be maintained for two weeks (Rahman & Rahman, 2005).

Once the 20mg/day level is reached, the dosage is lowered by 2.5mg per week.

Then, when the dosage reaches 10mg/day, it is reduced by 1mg every month depending on the symptoms and test results (Schmidt, 2006).

Most patients remain on corticosteroids for 1-2 years, although some may require long-term steroid treatment (Schmidt, 2006; Piptone et al., 2005).

The reason that treatment of GCA is usually short in duration is because GCA is a self-limiting disease for most patients (although the mechanism for this limitation is unknown) (Azhar et al., 2005; Schmidt, 2006).

Longer corticosteroid treatment is typically required for patients with more severe GCA; these patients usually have cytokine levels (such as TNF-α) above most GCA patients (Hernandez-Rodriguez et al., 2004).

[www.bio.davidson.edu]

ECG Quiz

2009-01-05T05:30:00.001-08:00

This is a 63 year old Chinese lady who presented with dizziness.

1. What does the ECG show ?

2. What is the treatment ?

Neurofibromatosis

2008-12-21T00:18:00.000-08:00

Station 5 PACES spot diagnosis in skin station ! Remember the criteria of diagnosis, so do not forget to check for Rinne/Weber if there is a tunning fork nearby and also ask for permission to ask about family history.

Table 2 : Criteria for Neurofibromatosis

Type 1 (Von Recklinghausen’s Disease)

Type 2

· Six or more café-au-lait spots, the greatest diameter of which is more than 5 mm in prepubertal patients and more than 15 mm in postpubertal patients

· Two or more neurofibromas or one plexiform neurofibroma. Plexiform neurofibroma is considered by some to be a defining lesion of neurofibromatosis type 1

· Frecking in the axilla or inguinal region (Crowe’s sign)

· Optic glioma

· Two or more Lisch nodules(iris hamartoma)

· A distinctive osseous lesion such as sphenoid dysplasia or thinning of long bone cortex with or without pseudoarthroses

· A parent, sibling or child with neurofibromatosis according to the above criteria

· Bilateral eight cranial nerve palsy confirmed by CT or MRI

· A parent, sibling or child with neurofibromatosis type 2 and either unilateral eight nerve mass or any two of the following : neurofibroma, meningioma, glioma, schanoma or juvenile posterior subcapsular lenticular opacity

Aortic Dissection

2008-12-11T04:13:00.000-08:00

An interesting case for medical students which I experienced today. I was running the medical clinic when one of the HOs informed me that there is a case needed to be seen in the Echo room.
It was a 64 year old Malay lady who is a known case of hypertension for about 30 years, presented with shortness of breath for 2 days. Clinically she had raised JVP, bibasal crepitations in the lungs and was tachypnoeic. BP 138/80(on antihypertensives) - almost the same the other side. no radio radial or radio femoral pulse.
Basically she had symptoms of congestive cardiac failure.
ECG - sinus tachycardia
CXR - upper lobe divergence, cardiomegaly and widening of the mediastinum
Echo revealed a flap from the ascending aorta to the arch and descending aorta suggestive of Type A aortic dissection EF 40%
She was immediately sent for CT angiogram of thorax and referred to the cardiothoracic.

Discoid lupus

2008-11-25T08:04:00.000-08:00

A young lady in station 5 in MRCP or short case in medical students with these skin lesions on the face can only be discoid lupus. As have been mentioned before, discoid lupus is one of the criteria for the diagnosis of SLE. There is atrophy with scarring and hyperpigmented lesions on the face. Do not forget to look at the hair and you will notice scarring alopecia.
I saw this young lady in the combine clinic.

Non medical Books

2008-11-08T00:20:00.000-08:00

Well, these would be useful for medical students. If you are interested, pls drop me an email at thienthienlim@gmail.com. I hope I don't need them anymore !

These books are simple to read.

Wallenberg syndrome

2008-11-06T02:38:00.000-08:00

A common case but may be underdiagnosed. I was informed by my fellow colleague regarding this interesting case. This patient is a 67 years old Indian man who is a known case of hypertension and diabetes mellitus for the past 10 years. He presented with difficulty in swallowing for the past 2 days associated with unsteady gait.
From the video, you will notice the following :
1) Patient is on a ryles tube and there is hoarseness of voice
2) R Horner's syndrome (miosis and ptosis seen)
3) Lack of movement of the R soft palate causing uvula pulled to the L
4) Reduced pin prick of the R face (inconsistent when I tested for this)
5) Bilateral cerebellar signs
6) Reduced pin prick L half of the body

This patient has R posterior inferior cerebellar infarct (PICA) also known as Wallenberg syndrome. This common stroke is caused by infarction of a wedge of lateral medull lying posterior to the inferior olivary nucleus. Let me try to explain the signs -
1) Nucleus ambiguus and fibers of IXth and Xth CN
2) Descending synpathetic tract
3) Nucleus ambiguus and fibers of IXth and Xth CN
4) Descending tract and nucleus of the V nerve
5) R cerebellar - ?restiform body, cerebellar hemisphere, olivocerebellar fibres, spinocerebellar tract, L cerebellar - patient also had an old infarct at the L cerebellar hemisphere(encephalomalacia from the CT scan)
6) Spinothalamic tract

Thanks to my radiologist, we will proceed for a CT angiogram soon.

Koebner phenomenon

2008-10-31T05:00:00.000-07:00

I remember this sign very well since I was a medical student. When I was sitting for the MRCP exam, I was told that most candidates will get psoriasis as a case in Station 5. However, not all will get a 4/4. To get 4/4 you need to shine among your other colleagues who are taking the exam at the same time.
So, remember that when you see a patient with psoriasis, always look for this sign which will be at any place with a trauma or scar.
The Koebner phenomenon, also called the isomorphic response, refers to the appearance of lesions along a site of injury.
The next question is what lesions causes Koebner phenomeonon. You need to memorise these
1) psoriasis
2) lichen planus
3) warts
4) molluscum contagiosum
5) vitiligo
There are a few more which are not so common

MRCP Part 2a Written

2008-10-20T02:30:00.001-07:00

This is a very good book for Part 2a Written. I won't be using it anymore. So, for those who are interested in this book, you can write to me at thienthienlim@gmail.com. I hope the person who is buying it would be sitting for the Part 2a Written as it is very useful for that part. Btw, you will only find this book out of Malaysia and I actually bought it in Singapore.

Necrobiosis Lipoidica Diabeticorum

2008-10-12T06:21:00.000-07:00

This patient has a sharply demarcated oval plaque over the shin. The lesion has shiny atrophic surface and a waxy yellow centre and brownish-red edges.
The diagnosis is necrobiosis lipoidica diabeticorum.

It is associated with diabetes
Differential diagnosis include
Granuloma annulare
Nodular vasculitis
Localised scleroderma/sarcoidosis

Treatment includes steroids(topical or local injection), severe cases can be treated with excision and skin grafting.

Other skin lesions in diabetics :
Diabetic dermopathy
Infective(Boils, candidiasis)
Foot/leg ulcers
Vitiligo
Fat atrophy/hypertrophy
Xanthomas
Acanthosis nigricans
Peripheral anhidrosis
Chlorpropamide alcohol flush

Hypocalcaemia

2008-10-12T05:58:00.000-07:00

I am sure there are many medical students who have read about this over and over again but may not have seen it. I take this opportunity to share one of my patients who has hypocalcaemia secondary to Albright Hereditary Osteodystrophy(very very rare cause) and in paeds. Actually he is followed up in paeds and was incidentally admitted to my ward because of low calcium. I elicited Chvostek's sign in him and immediately treated his hypocalcaemia

Symptoms

Symptoms generally correlate with the magnitude and rapidity of the fall in serum calcium: mild hypocalcaemia (2.00-2.12 mmol/l) can be asymptomatic whereas acute symptoms of neuromuscular irritability can develop in the more severe form(<1.9>

Paraesthesia (usually fingers, toes and around mouth)
Tetany
Carpopedal spasm (wrist flexion and fingers drawn together)
Muscle cramps

Signs

Chvostek's sign (tapping over facial nerve causes facial muscles to twitch) Note: this may be present in some normocalcaemic individuals. (refer video)
Trousseau's sign (carpopedal spasm after inflating a BP cuff on the upper arm) (refer video)
Seizures
Prolonged QT interval which may progress to VF or heart block
Laryngospasm
Bronchospasm

With prolonged hypocalcaemia

Sub-capsular cataract
Papilloedema
Abnormal teeth
Ectopic calcification (for example, in basal ganglia may cause extrapyramidal neurological symptoms)
Dementia and confusion

Aetiology

Causes of true hypocalcaemia fall into two main classes:

With low PTH levels (hypoparathyroidism)

Parathyroid agenesis- alone or along with other abnormalities e.g. Di George syndrome
Parathyroid destruction- due to surgery, radiotherapy, infiltration by metastases or systemic disease
Autoimmune
Reduced parathyroid secretion - due to gene defects, hypomagnesaemia, neonatal hypocalcaemia (may be due to maternal hypercalcaemia), hungry bone disease (after parathyroidectomy), mutation in calcium-sensing receptor.

With high PTH levels (secondary hyperparathyroidism)

Vitamin D deficiency- due to nutritional lack, malabsorption, liver disease, receptor defects
Vitamin D resistance (rickets)- renal tubular dysfunction (Fanconi's syndrome) or receptor defect
PTH resistance - pseudohypoparathyroidism, hypomagnesaemia

Important other causes

Hyperventilation
Drugs- calcium chelators (citrate in blood transfusion); bone resorption inhibitors (bisphosphonates, calcitonin, plicamycin); drugs affecting vitamin D (phenytoin, ketoconazole), foscarnet
Acute pancreatitis
Acute rhabdomyolysis - usually in relation to crush injuries
Malignancy - tumour lysis(following chemotherapy) or osteoblastic metastases (most common in prostate and breast cancers)
Toxic shock syndrome

Commonest causes are hypoparathyroidism (frequently following surgery), vitamin D deficiency or abnormal metabolism, renal failure, hypomagnesaemia.
Hypocalcemia is extremely common in patients in hospital and correlates with the severity of their illness.³

Differential diagnosis

	Serum phosphate	Serum PTH	Serum ALP	Other
Renal failure	Raised	Raised	Raised	Raised creatinine
Hypoparathyroidism	Raised	Low/undetectable		Normal Vitamin D metabolites
Pseudohypoparathyroidism	Raised	Raised
Vitamin D deficiency or malabsorption	Low	Raised	Raised	Raised 25 (OH)D3 levels

Hypoalbuminaemia - correct for albumin
Consider drug therapy, malignancy, acute pancreatitis and rhabdomyolysis

Investigations

Is the patient really hypocalcaemic? (Ideally take fasting blood specimens, uncuffed -remove tourniquet after needle in vein, but before taking blood sample). Ensure use an adjusted calcium value
Exclude renal failure (check U&Es), acute pancreatitis (check amylase), rhabdomyloysis (check serum CK)
Estimate serum magnesium
Estimate serum PTH
Evaluate Vitamin D metabolism

Always assess the patient clinically. Patients vary: some may be symptomatic within the normal reference range since there are narrow individual ranges within the normal reference range.

Management

Acute hypocalcaemia

Treat where symptomatic (seizures, tetany) or at high risk of complications with a serum calcium <1.90>
Give calcium gluconate IV 10 ml (2.25 mmol) of calcium gluconate 10% by slow injection. Repeat as necessary or follow with infusion of calcium gluconate 10% infusion - 40 ml (9 mmol)/24 hours.
Monitor serum calcium concentrations regularly to judge response.
If likely to be persistent, give vitamin D by mouth.
If hypomagnesemic, necessary to correct magnesium level before the hypocalcaemia will resolve.

Extracted from http://www.patient.co.uk/showdoc/40001110/

Bitemporal hemianopia

2008-10-04T03:36:00.000-07:00

When I was in UK, I attended a PACES course. There were 3 patients whom I was asked to examine the visual fields and the findings were bitemporal hemianopia. They also had a scar as shown above. In fact, they had craniopharyngioma which has been operated via a transfrontal approach. You don't always get a clear scar like this in the exam. So, sometimes you have to look in between the hairs for the scar.

Where is the lesion ? Optic chiasm

If you are asked to examine the eyes,
1) Inspection for scars (transfrontal and transphenoidal)
2) Examine the visual acuity with a Snellen chart
3) Test the visual fields (you will find bitemporal hemianopia)
4) Check light reflex and look for RAPD(relative afferent pupillary light reflex or Marcus Gunn pupil), accomadation reflex
5) Check eye movements
6) Do a fundoscopy ( look for optic atrophy, particularly if there is RAPD)
7) Look for a medic alert bracelet
8) Look for other features of endocrinopathy eg acromegaly, Cushing's syndrome which should also have been picked up during inspection

The other causes of a chiasmal lesion include pituitary adenoma, meningioma, aneurysm, glioma

Lou Gehrig

2008-09-28T06:50:00.000-07:00

You will know Lou Gehrig if you are a baseball fan or a Neurologist. Lou Gehrig whose name has been given to Amyotrophic lateral sclerosis was an "ironman" in baseball unfortunately died of ALS.
Amyotrophic lateral sclerosis is a type of motor neuron disease.
What you need to know in MRCP is that if you get a patient with mixed upper and lower motor neuron with no sensory involvement, you may be dealing with MND. Also if you see fasciculations - MND is high on the list. Of course, don't forget cervical myelopathy and multifocal motor neuropathy with conduction block as differential diagnosis.

The other possibility in exam is that you are given a patient with bulbar(as in the picture showing fasciculations and wasting of the tongue) or pseudobulbar palsy and one of the underlying aetiology would be MND.

Remember - The lesion is at the anterior horn cell
(first principle of neurology - Where is the lesion ?)

ECG for medical students

2008-09-19T21:26:00.001-07:00

40 years old man with palpitation

What does the ECG show ?

What are the further investigations ?

Outline the treatment plan.

Proximal myopathy 2

2008-09-17T04:55:00.000-07:00

Common exam question.
Attached is a video of my patient with proximal myopathy. Without the bed, he would show a classical Gower sign.
What is important is to determine the cause for the proximal myopathy.
In the exam, think of the major groups !

1) Muscular Dystrophy - normally Beckers cause Duchenne would be dead by then unless you are sitting for a paeds exam.
2) Polymyositis/Dermatomyositis
3) Endocrinopathies - Acromegaly, Cushing's, Thyrotoxicosis... look for features of those
4) Metabolic causes- Hypokalaemic periodic paralysis...
5) Myasthenia gravis

Those are the common ones.

Remember also to look for the muscle biopsy scar which is normally at the biceps or quadriceps.
There is no sensory involvement as the pathology is the muscle or neuromuscular junction.

Remember the investigations -
CK
Muscle biopsy
EMG

Treatment would depend on the underlying cause.

Refer to previous post on proximal myopathy

3rd nerve palsy

2008-09-11T07:08:00.000-07:00

Neuro-opthalmology always amazes me.

In this patient, there is L 3rd nerve palsy with sparing of the pupil - medical 3rd nerve palsy

Commonest cause are diabetes mellitus and hypertension.

When you get medical 3rd nerve palsy, check for diplopia then other cranial nerves. If only the 3rd nerve involve, test BP and blood glucose.

Other causes include - MS, trauma, collagen vascular disorder, syphilis,etc

It is wise to check for long tract signs and cerebellar signs.

Remember the fancy names ?

Weber syndrome - ipsilateral 3rd nerve palsy with contralateral hemiplegia (lesion in midbrain)

Benedikt's syndrome - ipsilateral 3rd nerve palsy with contralateral involuntary movements such as tremor, chorea and athetosis (lesion in red nucleus of midbrain)

Claude's syndrome - ipsilateral oculomotor paresis with contralateral ataxia and tremor( lesion in 3rd nerve and red ncleus)

Nothnagel's syndrome - unilateral oculomotor paralysis with ipsilateral cerebellar ataxia

To differentiate between central or peripheral - suspect central if unilateral 3rd nerve palsy with superior rectus palsy and bilateral partial ptosis/bilateral 3rd nerve palsy

Medical students : remember this !

SO4 LR6 - superior oblique by 4th CN, lateral rectus by 6th CN, the rest 3rd CN

Splenomegaly

2008-09-10T09:45:00.000-07:00

Never rush to examine the patient. Always remember the first few steps. Firstly, always introduce yourself to the patient then shake hand (except in Rheumatology) then ask the patient permission for examination.
The next step is to position the patient. Then it will be to start with inspection.
For the abdomen station, inspect at the end of the bed. This is a very crucial step. If you notice in the above patient which was taken during a medical student exam last year, you could actually get the diagnosis. There is an obvious swelling at the L hypochondriac region and if you are sitting for a medical exam, it must be the spleen or the L kidney.

The favourite questions for medical students :
What are the causes of massive splenomegaly ?

Malaria
Chronic myeloid leukaemia
Myelofibrosis
Kala azar (mention this last if you are in Malaysia or places where it is not endemic)
Gaucher's disease
Thalassaemia (though some would classify as mild to moderate)

How do you differentiate a kidney from a spleen ?

Kidney - ballotable, moves inferiorly, resonant on percussion, able to get above it, traube space resonant
Spleen - not ballotable, moves inferomedially, dull on percussion, unable to get above it, splenic notch, traube space dull

The above patient has CML with massive splenomegaly !!

MRCP Book

2008-09-06T20:41:00.001-07:00

This is quite a good book that I used in the MRCP PACES during my 3rd attempt. It is point form and gives very good examples especially in the history and communication section.
If you are interested to get it from me for a low rate, email me at thienthienlim@gmail.com.

You may still need to read in PACES although the key word is PRACTISE !!!

Normal Pressure Hydrocephalus

2008-09-06T02:10:00.000-07:00

This 70 years old gentleman presented with difficulty in walking for the past 3 years and recently has urinary incontinence. He also has poor memory for the past 1 year.

Favourite question in MRCP Part 1 and 2a(normally may show you a CT brain with hydrocephalus)

Clearly the triad of NPH are DIA(dementia, incontinence and ataxia)

The gait shown is an apraxic gait which sometimes mimic a gait in Parkinsonism.

The CT brain shows hydrocephalus and an LP done would normally be on the high normal about 15 to 20 cmH2O. The gait improved after CSF drainage.

Treatment would be by inserting a ventriculoperitoneal shunt (VP shunt)

Communication skills - Break Bad News

2008-09-02T03:34:00.000-07:00

In the MRCP PACES exam, the commonest case that one would get is Breaking bad news !
I must pay tribute for this section to Dr. Kok Lai Sun, Dr. Yoon CK and Dr. Ong Eng Eng who actually trained me in this till I got a 4/4 in my PACES which then made me pass, if not I used to be something like the cartoon above (Malaysian style).

Example :

Candidate information
You are a medical SHO on call for the coronary care unit(CCU).
Please read the scenario below. You may make notes on the paper provided. When the bell sounds enter the examination room to begin the consultation.

Mrs Tan PS
Age 55 years old
Re : Husband, Mr Tan PS, 60 years old

You are asked to talk to Mrs Tan PS regarding her husband, Mr Tan PS who was a 60 years old man who was admitted to the CCU on the previous evening, after experiencing an acute myocardial infarction. Prior to this he had been fit and well. He was a smoker and had hypertension for the past 10 years. Mr Tan had been thrombolysed and treated appropriately. However, during the night he had developed further chest pains and had a cardiac arrest from which he could not be resuscitated, despite a prolonged resuscitation, and died. Mrs Tan was informed regarding the deterioration through the phone but does not know that Mr Tan has passed away. You are to break the bad news to Mrs Tan.

You have 14 minuted to communicate with the patient followed by 1 minute reflection before discussion with the examiners.

How would you approach this type of scenario ?

Greet Mrs Tan and introduce yourself
Enquire if anyone else would like to be around during the conversation (such as other family members)
Enquire what she knows about Mr Tan and her expectations
Explain briefly on what prompted the admission and she feels he is progressing
'Fire a warning shot' (this is very important) - eg. During the night, Mr Tan had another chest pain and possibly another heart attack. Pause after that
Break the bad news. Go on to explain that Mr Tan's heart stopped beating(after another episode of heart attack). Explain that despite efforts of the medical team, he passed away
Pause and let the news sink in - let Mrs Tan express the shock and sadness, offer tissue if she cries
Be EMPATHETIC
Don't speak to much but be empathetic - such as 'Are you ok to go on' or ' I know this must be hard for you...'
Answer her questions
Close the interview

L LMN 7th CN palsy

2008-08-31T19:28:00.000-07:00

One of the most common cranial nerve examination in MRCP and Medical student exams !

Look at this patient's face and proceed with the necessary.

I remember that when I was practising with eMRCPian before my MRCP PACES exam, he used to tell me that do the necessary and don't examine the cranial nerves from I to XII which would normally be done by most medical students.

It is obvious from inspection that there is loss of nasolabial fold on the left.
Start with cranial nerve VII

Loss of wrinkling of the forehead, unable to close the L eye tightly, unable to blow the cheeks, mouth deviated to the right on showing the teeth
Look for Bell's phenomenon - upward movement of eye and incomplete closure of eyelid when the patient attempts to shut the eyelids

After establishing that it is LMN 7th CN palsy, next we have to see whether other cranial nerves are involved.

Check the III, IV, VI CN by checking the eye movement, a CP angle tumour can extend to involve these cranial nerves or in cases of NPC where you get multiple CN involvement
Check the V cranial nerve esp corneal reflex (remember that afferent is V and efferent is VII for corneal reflex)
Check the VIII cranial nerve - will be involved in CP angle tumour
You can check other cranial nerves quickly - IX,X,XI,XII
It won't be necessary to check the CN I or II

Next, we need to establish the cause if it is solely the VII LMN 7th CN involved.

Shine a torch into the ear(the site of the 7th CN palsy) to look for vesicles in Ramsay Hunt syndrome
Examine the parotid glands for parotid enlargement (remember that the 5 branches of the 7th nerves comes out here - Used to remember "Clincal examination by Talley, O' Connor" which mentioned Two Zebras Bit My Car - Temporal, Zygomatic, Buccal, Mandibular, Cervical)
Check for lymph nodes enlargement - NPC
Check also for cerebellar signs of the upper limbs (CP angle tumour)

Offer to check the taste of the anterior 2/3 of the tongue and to look for hyperacussis.

For medical students, try to remember the pathway of the 7th cranial nerve and the branches of it.

Frank's sign

2008-08-25T23:48:00.000-07:00

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.

For those who are medical students, if you get a case of Ischaemic heart disease or IHD, please look for this in addition to xanthalesma and corneal arcus in your exam.

For MRCP PACES candidates, if you still have not heard of this, you have not read enough of An Aid to the MRCP PACES by R.E,J Ryder, M.A Mir & E.A Freeman. It is on page 14 Section B on the 3rd edition and if I remember correctly it is in the first few pages in the 2nd edition when I read it long time ago during my medical student days.

Lower limbs and Guillain Barre syndrome

2008-08-07T22:00:00.000-07:00

This is a low power image of a peripheral nerve in GBS. It has been stained with a myelin stain (pink). Note the large areas of myelin loss in the center

The interesting about Neurology is that the history(eg pt with headache) & examination is still plays a very important role. In cardiology, Echo has sort of replaced cardiac examination, U/S abd and CT abd has sort of replaced gastroenteralogy cases and chest radiograph and CT has sort of replaced respiratory examination.
Well, I say sort of because it should not be the way and physicians and all doctors should be pasionate about the power of history taking and physical examination.
You may say that MRI brain has replaced Neurology but it is totally untrue because the most important question in Neurology is where is the lesion ? So, if you MRI the brain for a Guillain Barre syndrome then you are in the wrong direction !
Which now brings me to the topic of to locate the lesion

You are asked to examine a 33 years old man with weakness of the lower limbs in the exam.
How to start ?

Inspection - wasting of the thighs, no fasciculations, no scars
Tone - reduced bilaterally
Power - 2/5 distally and 3/5 proximally
Reflexes - absent bilateral knee and ankle reflexes
Plantar response - downgoing bilaterally

Cerebellar examination of lower limbs not able to be done in view of the weakness

Sensation - reduced pin prick bilaterally up to the knees

Gait unable to be test due to the power

SO, the first conclusion you should make is
this patient has LOWER MOTOR NEURON lesion of the lower limbs with peripheral sensory neuropathy

Next step is to locate the lesion.
It is anywhere from the anterior horn cell , nerve roots, plexus, peripheral nerve, neuromuscular junction, muscle.
It is not the ant horn cell or neuromuscular junction because of sensory involvement. It is at the peripheral nerve because of predominant distal neuropathy with distal sensory involvement.

So, this patient has peripheral motor sensory neuropathy (predominant motor).
Next are the causes of predominant motor peripheral neuropathy

Causes include :
Guillain Barre syndrome (acute)
Chronic inflammatory demyelinating neuropathy (chronic)
Charcot Marrie Tooth/Hereditary motor sensory neuropathy
Lead poisoning
Acute intermittent porphyria

This patient actually has Guillain Barre syndrome.
So, you can see how important your examination is and from there you can actually investigate treat the patient. MRI brain will be useless.
You could do an LP to look for cytoalbuminaemic dissociation and a nerve conduction study.

If you suspect GBS, examine the pulse for tachycardia(autonomic dysfunction) and cranial nerves(weakness of the facial muscles).
Also you could do a vital capacity to look for respiratory involvement.

Treatment would be IVIG or plasmapheresis (more effective if given early)

Tuberous sclerosis

2008-08-07T06:36:00.000-07:00

This young man has epilepsy and mental retardation.
The picture shows Shagreen patch(leathery skin patch over the back) and adenoma sebaceum(shiny papules at the nasolabial fold), classical of tuberous sclerosis.
The 3 neurocutaneous syndromes that medical students and MRCPian need to know include neurofibromatosis, tuberous sclerosis and Sturge Weber syndrome.

Tuberous sclerosis is an autosomal dominant disease characterised by multiple organ hamartomas.

Skin - Adenoma sebaceum(angiofibromas), subungal fibroma, Shagreen patch, ash leaf macules
Renal - Angiomyolipomas
Cardiac - Rhabdomyosarcomas
CNS - Subependymal nodules, Cortical tubers, benign white matter lesions, subependymal giant cell astrocytoma
Eye - retinal phakomas

If you get this in the exam, dont forget to ask about seizures and mental retardation !

Also I just advised my houseman just now that if you see a patient in the ward that came in for seizure, do not forget to look for neurocutaneous signs.(was previously thought to me by my consultant neurologist)
THE EYE DON'T SEE WHAT THE MIND DON'T THINK !(was told to me by my lecturer)

Nail changes in Psoriasis

2008-08-04T08:38:00.000-07:00

Psoriasis as I have mentioned is an important skin disorder - both medical students and MRCP candidates have to know.

The nail changes in psoriasis are :
1) Pitting of the nails
2) Onycholysis
3) Discolouration (Oil drop sign)
4) Ridging
5) Subungal hyperkeratosis

The arthritis in psoriasis are :
1) Oligoarthritis
2) Distal asymmetrical arthrtis
3) RA like arthritis
4) Ankylosing spondylitis like arthritis
5) Arthritis mutilans

The types of psoriasis are :
1) Chronic plaque
2) Guttate
3) Pustular
4) Erythrodermic
5) Inverse

Remember all in 5.....these are the few favourite questions

Heart murmurs

2008-08-03T08:45:00.000-07:00

The heart murmurs are something very fascinating ! At one time, I found it so fascinating that I thought of becoming a cardiologist. But it seems now that echo becomes the trend. Medical students need to know the murmurs well, not forgetting those who are sitting for the MRCP exam.

Pansystolic murmur at apex - axilla = Mitral regurgitation
Mid diastolic murmur at apex, best on L lateral position = Mitral stenosis
Early diastolic murmur at LSE, best on sitting up on expiration = Aortic regurgitation
Ejection systolic murmur at aortic, radiating to the carotids = Aortic stenosis

Pansystolic murmur at tricuspid, best on inspiration = Tricuspid regurgitation

Pansystolic murmur at LSE, 3rd intercostal space = Ventricular septal defect(VSD)
Ejection systolic murmur at pulmonary area, with wide fixed split S2 = Atrial septal defect(ASD)
Continuous murmur = Patent ductus arteriosus (PDA)

Memorise it medical students !!

Internuclear opthalmoplegia

2008-08-02T03:37:00.001-07:00

I am currently attending a MS workshop organised by KL GH with Bayer in Cyberview Lodge Resort & Spa. Nice place !

Well, multiple sclerosis is a common exam question and we discussed a little in the optic atrophy topic.

Remember that it is very common to be asked to examine the cranial nerves. Neuroopthalmology can be very interesting.

The above picture shows that the patient is looking to the right. There is failure of adduction of the L eye and nystagmus on the R eye.

The diagnosis is L INO (remember that the pathology is at the site of the failure if the abducted eye)

If you get bilateral INO - it is almost always MS especially when you see a young lady.

So if you get INO, remember to check for RAPD, Lhermitte's by flexing the neck, cerebellar signs and offer to do a fundoscopy to look for optic atrophy. You can also check the lower limbs for upper motor neuron signs in transverse myelitis and if you have that it is surely MS.

Where is the lesion ?

MLF - medial longitudinal fasciculus

Remember the pathway of PPRF and the 6th nerve. I am sure you can figure out the rest.

What is the criteria used for MS ?

Mc Donald's - previously it was Poser criteria

How would you investigate MS ?

MRI brain/spinal cord, neurophysiology study - VEP,SSEP, BAER, LP for oligoclonal band and IgG

McDonald's criteria focusses a lot on MRI.

What would you treat the patient in the acute phase ?

IV methylprednisolone

What is the long term treatment to reduce relapses ?

Beta interferon or glatiramer acetate

Rheumatoid arthritis

2008-08-01T09:32:00.000-07:00

A very common exam question in undergraduate exam up to MRCP PACES.
Sing the song before you go into the exam hall and you'll be confident coz they are almost the same. Don't be over confident though coz the examiner is like the 'Joker' in Batman - you need to outsmart him, he is not that straight forwaard. You have to be the DARK KNIGHT !!

This patient has bilateral symmetrical deforming arthropathy involving the MCP/PIP joints but sparing the DIP joints.
There is Z deformity of the thumb, boutonnière's deformity and swan neck deformity
Tinel sign is positive suggesting carpal tunnel syndrome.
There is also limited movement of thumb abduction and opponens.
There are no nail changes or rashes to suggest RA like psoriatic arthropathy.
There is Rh nodules.
Functinally she can still write and unbutton her shirt.
There is no evidence of episcleritis/scleritis/scleromalacia perforans and the lungs are clear(rule out Rh lung). I would like to examine the abdomen for splenomegaly in Felty's syndrome or hepatosplenomegaly in amyloidosis.

My diagnosis is that this patient has RA and it is inactive as there joint swellings are hard suggesting subluxation and the joints are not warm of tender.

Questions :
What are the causes of anaemia in RA ?

What are the poor prognosis factors ?

How would you investigate this patient ?

What are the options of treatment ?

Erythema ab igne

2008-07-31T06:14:00.001-07:00

Interesting article from NEJM. It is a common MRCP question for Part 1 & 2a. Do not forget its relationship with hypothyroidism.

This patient has L knee pain.

This reticular, reddish-brown, pruritic, nontender, macular, nonblanching discoloration around the medial aspect of the left knee, with a few superficial erosions, is most consistent with erythema ab igne. This patient had repeatedly applied a heating pad to his left knee in the preceding weeks to relieve discomfort from osteoarthritis.

Optic atrophy

2008-07-30T00:19:00.001-07:00

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.

Proximal myopathy

2008-07-23T04:51:00.000-07:00

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

The above patient with proximal myopathy also has features of Cushing's syndrome. Remember that Cushing's syndrome can cause proximal myopathy but also do not forget that steroid use for polymyositis/dermatomyositis can also cause Cushing's syndrome.

How do you differentiate polymyositis, dermatomyositis and inclusion body myositis ?

Polymyositis Dermatomyositis Inclusion body myositis

Sex F>M F>M M>F

Age Adult Childhood & Adult Elderly > 50 years old

Rash Yes No No

Distribution of weakness Prox > Distal Prox > Distal Prox = Distal,

predilection for

finger/wrist flexion,

knee extensors

CK incr (up to 50x) N or incr (up to 50x) N or mildly incr (<10

x N)

Muscle biopsy amyloid deposits

Response to

immunosupressive Yes Yes No or minimal

EMG myopathic myopathic myopathic/neuropathic

PACES course 13/14 Sept 2008

2008-07-21T04:17:00.000-07:00

This picture was the first picture that came out when I typed PACES in google. Well, I guess it just means that only a few steps and you'll also be there :)

Thanks for the overwhelming response for the PACES course registration. All the seats for the PACES course are filled up.

I am also very happy as I have got several professional tutors who have confirmed coming for the course eg. Prof Richard, Prof Amir, Prof Malik, Prof Raymond, Dr. Haniffah, Prof Rashid, Dato' Dr. Chandran, ....many others who will surprise you on that day.

There are some who have asked regarding the attire on that day. It would be formal and I would advise you to wear as though you will be going for the PACES exam(well, don't worry coz the whole place is air-conditioned)

Leprosy (Hansen's Disease)

2008-07-17T07:25:00.000-07:00

Examine this patient's feet

Look at this patient's face and examine him

You might this case in Malaysia PACES center, station 5.

This patient has leonine facies (face features resemble a lion) and the ear lobe is thickened as well.

Note: The other differential for leonine facies is cutaneous T cell lymphoma.

There is presence of amputated R index finger and L 4th and 5th toe. The small muscles of the hands are wasted.

There is evidence of sensory peripheral neuropathy and the ulnar and common peroneal nerves are thickened on palpation.

The overall picture shows that this patient has lepromatous leprosy complicated by severe neuropathy.

Questions:

1) How would you classify leprosy ?

According to Madrid classification system, it is classified into Tuberculoid, Bordeline and Lepromatous type.

However, WHO classify it into 2 types i.e. paucibacillary and multibacillary type for treatment purposes.

2) How would you investigate this patient ?

- Slit skin smear, skin biopsy

- Nerve conduction study for neuropathy as in this patient

3) How would you manage this patient ?

Start anti Leprosy agents - Clofazamine, Dapsone, Rifampicin

Screen other family members

Carotenaemia

2008-07-15T20:19:00.000-07:00

I saw this patient in the Medical clinic yesterday.
He is a 45 years old man with Follicular lymphoma who completed chemotherapy CHOP in 2006 with no B symptoms and no enlarged lymph nodes.
If you see him, you would think that he has jaundice. But, his sclera does not show that .

Further history reveals that he has been taking 3 carrots daily since after the chemo as was told to be good from his friends. Yup ! Carotenaemia.

What causes carotenaemia?
Excessive intake of carrots, and/or other yellow and green vegetables and citrus fruits are the usual cause of
carotenaemia (American spelling carotenemia). Carotene is the chief precursor of Vitamin A and is converted to
this in the mucosal cells that line the small intestine. Pancreatic lipase enzymes, bile salts, fat, and thyroid
hormone aid conversion and absorption. Thus carotenaemia is more likely in some diseases such as liver disease,
hypothyroidism and diabetes mellitus where this is impaired. In rare cases, a genetic defect in carotene
metabolism may also be a cause of carotenaemia, without requiring excessive intake of carotene.
Who gets carotenaemia?
Carotenaemia can occur at any age but is most common in young children fed large amounts of commercial
infant food preparations. These foods often contain carrots, pumpkin, squash, spinach and sweet potato, all of
which are high in carotene. Cooking, mashing and pureeing these foods make carotene more available for
absorption. Carotenaemia has also been found in vegetarians or food faddists who over-indulge in carrots and
oranges.
What are the clinical features?
Carotenaemia is characterised by yellow discolouration of the skin, particularly in areas where the horny layer is
thickened such as the soles and palms. It is also most evident on areas where subcutaneous fat is abundant. The
sclera (white outer coating of the eyeball) and mucous membranes (eyes, mouth, nostrils etc) are unaffected. The
presence of yellowing of the sclera usually means there is increased circulating bilirubin and is known as jaundice.

2nd MRCP PACES Preparatory Course

2008-07-15T09:08:00.000-07:00

The 2nd MRCP PACES Preparatory Course is finally in place. The organise, 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

Erythema nodosum

2008-07-14T06:20:00.000-07:00

Very frequent MRCP exam question, especially Part 1 & 2a, don't be surprised if it comes out in Station 5 PACES.

The picture shows erythematous nodules over the legs involving the shin. They are tender and elevated.
My diagnosis is that this patient has erythema nodosum.

You need to know the causes !

May even appear in history taking if you read Mir &Ryder PACES
Idiopathic/ unknown
Sarcoidosis
Streptococcal infection
Tuberculosis
Infections other than TB or strep - HIV...
Pregnancy or oral contraceptives
Drugs other than OCAs
Inflammatory bowel disease
Behcet's disease
Other

Dermatomyositis

2008-07-14T03:19:00.001-07:00

Skin station - common MRCP question. Also seen in Undergraduate medical exams. I remember seeing my first dermatomyositis patient in Sarawak General Hospital when I was a medical student in 3rd year and was told by the physician to remember the characteristic facies.

This patient has heliotrope rash(named after the above flower which I took the photo while I was in UK for my MRCP exam). He also has gottron's papules with proximal myopathy. There are no oral ulcers or arthritis to suggest mixed connective tissue disease. There is a biopsy scar at his R biceps.

What are the investigations you would perform ?
CK, EMG, muscle biopsy, anti Jo1

What is the definitive treatment ?
High dose steroids 1 mg/kg

What is the association ?
Internal malignancy eg NPC, GI, Breast, Ovary, Lung, mostly detected within 2 years

Marfan syndrome

2008-07-13T21:26:00.000-07:00

Always kept for exams for both medical students and MRCP exams.
Always look for this in the CVS station so you'll never miss it. It may also come out in Station 5 for MRCP candidates.

This patient is tall and has presence of arachnodactyly. There is positive wrist sign and steinberg sign. There is also presence of collapsing pulse and corrigan's sign. There is no evidence of disloaction of the lens. He has high arched palate and the chest does not show pectus excavatum or carinatum. There is no stigmata of IE.
The JVP is not raised and there is no pedal oedema. There is no scar on the precordium. The apex is displaced at 6th ICS at L MCL. No parasternal heave, no thrills. Normal 1st and 2nd HS. There is a Grade 3 EDM @ LSE best heard on expiration and sitting forward.

My diagnosis is that this patient has Moderate AR 2 to Marfan syndrome. I would like to look for other signs of AR eg Quincke, de Musset, pistol shot....

What's your differential diagnosis ?
Homocystinuria

What other valve lesions would you suspect in Marfan syndrome patients ?
MVP

What is the inheritance ?
AD

What investigations would you do ?
ECG, CXR, Echo

What is the Echo criteria for valve replacement in AR pt ?
symptomatic, LV end systolic diameter >5.5 cm or LVEF < 50%

If you are allowed to do one test for a patient with AR without Marfan, what test would it be ?
VDRL

Graves Disease

2008-07-12T22:25:00.000-07:00

Looks easy ? If a case looks easy in MRCP, always think again and do something to impress the examiners.

Examination :
Hands - Tremor, onycholysis, Acropashy, Warm sweaty palms
Pulse rate, Irregular to suggest AF ?

Proximal myopathy

Eyes - Exopthalmos, proptosis, Lid lag, lid retraction, Extraocular movements, chemosis

Neck - Scar, Goitre - Inspect, palpate for ? single nodule, multinodular, diffuse(most likely diffuse in Graves), percuss for retrosternal extension, auscultate for bruit

Limb - Pretibial myxedema, tendon reflexes

Well, if you got all those, I guess medical students can do all that.

So, you need to mention whether the disease is active or not.
Signs of activity - tremor, warm&sweaty palms, Thyroid bruit, Tachycardia

So mention the diagnosis as Graves disease and currently the disease is active as evidence by.....

Peutz-Jeghers syndrome

2008-07-11T23:30:00.000-07:00

I have never seen this till my practice for the MRCP exam. Well, there are some cases where you will never see before in your whole life except from atlas or websites and it appears for the first time during your MRCP examination. Don't get drawn back. Always stay calm and show the examiner that it is an easy case and talk confidently although you know nuts about it. Remember that the examiner cannot ask you much in the PACES exam because time is short and remember that they are physicians and not dermatologists !

There are small pigmented macules on the lips and buccal mucosa, suggestive of Peutz-Jeghers syndrome. I would like to ask the patient for any abdominal pain or previous history of GI bleed. I would also like to ask for family history of similar problem as it is autosomal dominant.

Peutz-Jeghers is associated with intestinal polyposis which are hamartomas and there is increased incidence of breast, ovarian and pancreatic malignancy.

Other differential diagnosis for this type of hyperpigmentation would include Addison's disease.

Psoriatic arthropathy

2008-07-10T22:30:00.001-07:00

If you think you see RA in MRCP exam, think again ! It may be Psoratic arthropathy RA like or it may also be mixed connective tissue disease.

Examine this patient's hands

This patient has psoriatic arthropathy (Rheumatoid arthritis like) as evidence by bilateral symmetrical deforming arthropathy involving the MCP and PIP joints bilaterally sparing the DIP joints. There is also erythematous plaques with silvery scales involving the hands, scalp, behind the ears, extensor surface of the legs and the trunk. There are also nail changes if pitting and subungal hyperkeratosis but no discolouration,ridging or onycholysis. There is a vertical scar over the R knee suggestive of R knee replacement. There is no evidence of Koebner phenomenon over the scar. There is limitation of movement of the hands but functionally she could still grip and hold a key.

What is this type of psoriasis and what are the other types ?

This is chronic plaque psoriasis and the others include guttate, inverse, erythrodermic, pustular psoriasis

What are the arthropathy of psoriasis ?

- RA like

- Oligoarthritis

- Distal asymmetrical

- Ankylosing spondylitis type

- Arthritis mutilans

How would you like to manage this patient ?

Multidisciplinary approach

Treat pharmacologically and non-pharmacologically

Pharmacologically - Systemic treatment in view of arthropathy and also skin involvement of > 70% eg Methotrexate, Coal tar for the scalp

Non-pharmacologically - physiotherapy, occupational therapy, avoid precipitating factors eg drugs - beta blockers, qunidine, lithium, stress,

What infections can precipitate psoriasis ?

Streptococcal

HIV

Beau's line

2008-07-10T03:33:00.000-07:00

I have stressed this to medical student before that nails are very important and in fact you can come to a diagnosis based on nails.
This is one of my patient in the haematology ward who came for chemotherapy for ALL(Acute lymphoblastic leukaemia).

The above shows Beau's line which is due to temporary arrest of nail growth from chemotherapy agent for the haematological malignancy.

Review from http://www.aafp.org/afp/20040315/1417.html

Nail Findings and Associated Systemic Conditions

Nail finding	Associated systemic conditions
Shape or growth change
Clubbing	Inflammatory bowel disease, pulmonary malignancy, asbestosis, chronic bronchitis, COPD, cirrhosis, congenital heart disease, endocarditis, atrioventricular malformations, fistulas
Koilonychia	Iron deficiency anemia, hemochromatosis, Raynaud's disease, SLE, trauma, nail-patella syndrome
Onycholysis	Psoriasis, infection, hyperthyroidism, sarcoidosis, trauma, amyloidosis, connective tissue disorders
Pitting	Psoriasis, Reiter's syndrome, incontinentia pigmenti, alopecia areata
Beau's lines	Any severe systemic illness that disrupts nail growth, Raynaud's disease, pemphigus, trauma
Yellow nail	Lymphedema, pleural effusion, immunodeficiency, bronchiectasis, sinusitis, rheumatoid arthritis, nephrotic syndrome, thyroiditis, tuberculosis, Raynaud's disease
Color change
Terry's (white) nails	Hepatic failure, cirrhosis, diabetes mellitus, CHF, hyperthyroidism, malnutrition
Azure lunula	Hepatolenticular degeneration (Wilson's disease), silver poisoning, quinacrine therapy
Half-and-half nails	Specific for renal failure
Muehrcke's lines	Specific for hypoalbuminemia
Mees' lines	Arsenic poisoning, Hodgkin's disease, CHF, leprosy, malaria, chemotherapy, carbon monoxide poisoning, other systemic insults
Dark longitudinal streaks	Melanoma, benign nevus, chemical staining, normal variant in darkly pigmented people
Longitudinal striations	Alopecia areata, vitiligo, atopic dermatitis, psoriasis
Splinter hemorrhage	Subacute bacterial endocarditis, SLE, rheumatoid arthritis, antiphospholipid syndrome, peptic ulcer disease, malignancies, oral contraceptive use, pregnancy, psoriasis, trauma
Telangiectasia	Rheumatoid arthritis, SLE, dermatomyositis, scleroderma

Tendon xanthomas

2008-07-08T07:14:00.001-07:00

This is a common MRCP exam question. My friend just got this 1 week ago when sitting for the exam in Singapore.

There are 2 differential diagnosis that you have to think about
1) Chronic tophaceous gout
2) Tendon xanthomas

The question is how to differentiate both of them. One simple test is that tendon xanthomas move with the tendon. So ask the patient to move the finger and feel the lesions and see whether it moves with the tendon.
Look also at the distribution of the deposits, in tendon xanthomas over the knuckles, elbows, knees, Achilles tendon. Look also for xanthalesma.
For gouty tophi, look at the ear lobes, feet, elbows.

Comment
Tendon xanthomas are seen in 75% of adults with familial
hypercholesterolaemia. They are intra-and extra-cellular
accumulations of cholesterol, noticed on extensor
tendons over knuckles, achilles, knee, and elbows. They
decrease with treatment of hypercholesterolaemia. They
are also seen in familial defective apo B100, type 3
hyperlipoproteinaemia, and sitosterolaemia

Reference
1. Mahley RW, Weisberger KH, Farese RV. Disorders of Lipid
Metabolism in Wilson JD, Foster DW, Kronenberg HM, Larsen
PR (eds). William’s Textbook of Endocrinology (9th ed).
Philadelphia, WB Saunders 1998; 23: 1099-1153.

Systemic lupus erythematosus

2008-07-07T23:13:00.000-07:00

For MRCP PACES candidates,
besides Psoriasis, please remember this as one of the most common exam questions.
I got this case in my 3rd attempt of PACES in Malaysia.

This patient has a malar rash. Describes as erythematous rash over the cheeks and bridge of nose and sparing the nasolabial folds. There is also presence of hypo and hyperpigmentation, however there is no follicular plugging.
My diagnosis is that this patient most likely has SLE and I would proceed to look for oral ulcers, discoid lupus, arthritis, alopecia, listen to the heart for pericardial rub, listen to the lungs for pleural effusion(serositis) and examine the abdomen for presence of hepatosplenomegaly. I would also like to look at the fundus for cytoid bodies.

Criteria for SLE
1) Malar rash
2) Discoid lupus
3) Photosensitivity
4) Oral ulcers
5) Arthritis
6) Serositis (Pleuritis/Pericarditis)
7) Renal disorder : Proteinuria >500 mg/d or cellular casts
8) Neurological disorder
9) Haematological disorder
10) Immunological disorder : anti dsDNA, anti Smith Ab, ACA/LA, false positive VDRL
11) ANA

Need 4 out of 11 criteria

What investigations would you perform to look for activity ?
ESR, C3, C4, CRP

What is the most common neurological manifestation ?
Psychosis

Splinter haemorrhage

2008-07-05T06:35:00.001-07:00

For medical students, always start examination from the periphery unless told not too in a short case. The nail is one of the most important clue. We saw clubbing previously and this is the diagram of a splinter haemorrhage.
The most common cause for splinter haemorrhage is trauma. Yes, it is not infective endocarditis. But you must not forget IE as one of the cause.

Can any medical students tell me in 'comments' other signs of infective endocarditis ?

The answer is
Osler nodes, Janeway lesion, Roth spot, clubbing.

Worth remembering !

Modified Duke criteria

Pathological criteria

Positivehistology or microbiology of pathological material obtainedat autopsy or cardiac surgery (valve tissue, vegetations, embolicfragments, or intracardiac abscess content)

Major criteria

Twopositive blood cultures showing typical organisms consistentwith infective endocarditis, such as Streptococcus viridansand the HACEK group OR
Persistent bacteraemia from two bloodcultures taken > 12 hours apart or three or more positiveblood cultures where the pathogen is less specific, such asStaphylococcus aureus and Staph epidermidis OR
Positive serologyfor Coxiella burnetti, Bartonella species, or Chlamydia psittaciOR
Positive molecular assays for specific gene targets
Positiveechocardiogram showing oscillating structures, abscess formation,new valvular regurgitation, or dehiscence of prosthetic valves

Minorcriteria

Predisposing heart disease
Fever > 38°C
Immunologicalphenomena such as glomerulonephritis, Osler's nodes, Roth spots,or positive rheumatoid factor
Microbiological evidence notfitting major criteria
Elevated C reactive protein or erythrocytesedimentation rate
Vascular phenomena such as major emboli,splenomegaly, clubbing, splinter haemorrhages, petechiae, orpurpura

Definite infective endocarditis

Pathological criteriapositive OR
Two major criteria OR
One major and two minorcriteria OR
Five minor criteria

Fundoscopy - DM proliferative retinopathy

2008-07-02T06:39:00.000-07:00

This is also one of the commonest MRCP exam question. Even medical students should know how to look at this.

When you reach this station, look around.
If you see a walking stick - Retinitis pigmentosa
If you see diabetic dermopathy- DM retinopathy(usually proliferative)
If you see an infusion pump - Grade 4 hypertensive retinopathy
If you see malar rash or Cushingoid facies - Optic atrophy

Sounds easy......but still one of the most feared exam station in PACES

The patient has DM proliferative retinopathy as evidence by multiple panphotocoagulation scars at the peripheral and also there is neovascularization. There are also dot blot haemorrhages and soft exudates.

Retinitis Pigmentosa

2008-06-30T06:40:00.001-07:00

Top 3 favourite MRCP PACES question besides Diabetic retinopathy and Optic atrophy !

There is widespread scattering black pigments resembling bony corpuscles. The macula is spared. There is tunnel vision. My diagnosis is Retinitis Pigmentosa.

Check the polydactyly, look out for obesity, bilateral ptosis, ichtiosis and also a ICD. Also check for cerebellar signs and hearing.

Causes :
Laurence-Moon-Biedel-Bardet syndrome (polydactyly, obesity)
Refsum's Disease (cerebellar ataxia, deafness, peripheral neuropathy, cardiomyopathy, ichtiosis)
Kearn's Sayre syndrome (opthalmoplegia, bilateral ptosis, heart block)
Hereditary ataxia (eg Friedreich's ataxia)
Abetalipoproteinaemia
Familial neuropathies

You should score if you get this case in MRCP exam !

Peripheral blood film 2

2008-06-29T20:18:00.000-07:00

This is a 40 years old Indian lady who was admitted with complains of abdominal swelling for the past 6 months. She also has loss of appetite. Clinically she has hepatosplenomegaly with a spleen of 10 cm below the L costal margin and a liver of 5 cm below the R costal margin at R midclavicular line.

A peripheral blood film done shown as above.

Question 1 :

What does the PBF show ?

What further investigations would you do ?

What are the other causes of massive splenomegaly ?

What is the definitive way to find the diagnosis ?

What is the treatment ?