Sunday, December 21, 2008


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 caf√©-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

Thursday, December 11, 2008

Aortic Dissection

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.

Tuesday, November 25, 2008

Discoid lupus

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.

Saturday, November 8, 2008

Non medical Books

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

These books are simple to read.

Thursday, November 6, 2008

Wallenberg syndrome

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.

Friday, October 31, 2008

Koebner phenomenon

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

Monday, October 20, 2008

MRCP Part 2a Written

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 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.

Sunday, October 12, 2008

Necrobiosis Lipoidica Diabeticorum

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
Fat atrophy/hypertrophy
Acanthosis nigricans
Peripheral anhidrosis
Chlorpropamide alcohol flush


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 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


  • 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

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
  • 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.


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

Saturday, October 4, 2008

Bitemporal hemianopia

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

Sunday, September 28, 2008

Lou Gehrig

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 ?)

Friday, September 19, 2008

ECG for medical students

40 years old man with palpitation

What does the ECG show ?

What are the further investigations ?

Outline the treatment plan.

Wednesday, September 17, 2008

Proximal myopathy 2

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 -
Muscle biopsy

Treatment would depend on the underlying cause.

Refer to previous post on proximal myopathy

Thursday, September 11, 2008

3rd nerve palsy

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

Wednesday, September 10, 2008


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 !!

Saturday, September 6, 2008


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

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

Normal Pressure Hydrocephalus

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)

Tuesday, September 2, 2008

Communication skills - Break Bad News

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
  • 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

Sunday, August 31, 2008

L LMN 7th CN palsy

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.

Monday, August 25, 2008

Frank's sign

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.

Thursday, August 7, 2008

Lower limbs and Guillain Barre syndrome

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

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)

Monday, August 4, 2008

Nail changes in Psoriasis

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

Sunday, August 3, 2008

Heart murmurs

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 !!

Saturday, August 2, 2008

Internuclear opthalmoplegia

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

Friday, August 1, 2008

Rheumatoid arthritis

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 ?

Thursday, July 31, 2008

Erythema ab igne

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.

Read More: New Engl J Med 356;9:e8

Wednesday, July 30, 2008

Optic atrophy

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)


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.


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.

Wednesday, July 23, 2008

Proximal myopathy

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

**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

Monday, July 21, 2008

PACES course 13/14 Sept 2008

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)

Thursday, July 17, 2008

Leprosy (Hansen's Disease)

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.


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

Tuesday, July 15, 2008


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
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

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

Monday, July 14, 2008

Erythema nodosum

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
Streptococcal infection
Infections other than TB or strep - HIV...
Pregnancy or oral contraceptives
Drugs other than OCAs
Inflammatory bowel disease
Behcet's disease


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