Clinical Skills

Respiratory Examination MRCP PACES

2009-09-09T00:19:00.000-07:00

We were teaching for MRCP PACES yesterday and had a patient with a common problem but the examination showed up common mistakes made by candidates in their approach to the examination of the respiratory system

The candidate was asked to examine the respiratory system and proceeded with what appeared to be a reasonable method. However, she did commence examination of the chest from the posterior aspect and after finishing the examination of the back of the chest she said she had concluded the examination and gave the findings.

She said that the patient was breathless at rest, was using oxygen via nasal prongs, there were no peripheral signs and the chest was normal apart from bilateral basal crepitations.

When asked the diagnosis she said that the patient probably had fibrosing alveolitis.

We then asked about other causes of bilateral basal crepitations and why it was not heart failure or brocnhiectasis or atypical pneumonia and these questions were difficult to answer as she had not looked at the JVP nor looked around for sputum pots or inhalers

We then re-examined the patient using ACES

The patient was propped up in bed suggesting dyspnoea and we mentioned some of the causes of dyspnoea (ACES for PACES page 245)

The height and weight were satisfactory and the skin was tanned all suggesting that the patient had been reasonably well till admission and was able to get about and possibly have a holiday

On examination of the head we that his face was flushed. We questioned the candidate about the cause of this and she came out with the possibility of the patient being a pink puffer(ACES for PACES page 249). At this point the possibility of COPD was raised. We also noticed flaring of the alae nasi further reinforcing our idea that the patient had respiratory distress(ACES for PACES page 250).

On examination of the hands we did not notice any clubbing but the peripheries were warm and there was a high volume pulse that was not collapsing

On examination of the neck we noted a raised JVP almost to the ear lobe with no predominant waveform. This raised the possibility of cor pulmonale or heart failure but as we were already going on the lines of COPD cor pulmonale was more likely (ACES for PACES page 256-257).

There was inspiratory descent of the trachea, more features showing us the extent of the dyspnoea.

The trachea was in the midline but the cricosternal distance was decreased. This further reinforced the idea the patient had COPD (ACES for PACES page 257).

On examination of the chest it was barrel shaped and there was little movement of the chest wall with respiration being predominantly abdominal (ACES for PACES page 258).

The respiratory rate was 26 per minute, more evidence of respiratory distress

The apex beat was difficult to palpate (ACES for PACES page 202).

Respiratory movements were equal on the two sided vocal fremitus unremarkable

Percussion not showed increased resonance with diminished cardiac and liver dullness. This added further weight to our diagnosis of COPD (ACES for PACES page 262).

Breath sounds were vesicular

There were a few crepitations at both bases but they were mostly mid-inspiratory and cleared with coughing (ACES for PACES page 264-265).

Heart sounds were soft

Diagnosis

COPD

Respiratory failure

Cor pulmonale

This case demonstrated very clearly how a methodical examination with evaluation of the findings at each step (ACES) makes diagnosis much easier than collecting all the signs and trying to recognise a pattern at the end

SOCRATES versus ACES mnemonic

2009-04-09T09:35:00.000-07:00

I was teaching a medical student this afternoon.
I discussed history taking with him. I asked him how he would analyse a patient’s symptoms and discussed analysis of pain.
He said he used the acronym SOCRATES and he proceeded to tell me the features he would ask for. The acronym was quite reasonable and he was able to name most features he would ask for in the analysis of symptoms.
I then discussed the mnemonic from ACES for PACES –Please Carefully Question This Method For Reliability and Resilience”- ACES for PACES page 22-24
He pondered this and said he would think about the two carefully as the ACES mnemonic seemed to be more comprehensive than the acronym he was using.
I then showed him how he could use the ACES mnemonic to analyse the pulse, murmurs, respiration and other functions of the body analysed on physical examination. ACES for PACES page 30-31
It is important to think about clinical skills and realise that a simple, common sense approach is all that is needed

Neurology for MRCP PACES

2009-02-27T01:06:00.000-08:00

We saw a very interesting case when teaching for PACES
After the initial examination and presentation of findings we went through the case again one step at a time with analysis to demonstrate how examination and interpretation should be done.
We initially looked at the dimensions of the lower limb and then looked at the skin (ACES for PACES page 417)
At this point we noted that the patient had trophic changes in the skin (loss of hair, callosities)
Immediately we thought that this could indicate a peripheral neuropathy.
Next we looked at the muscle mass and noted wasting of the muscles of both lower limbs. This made us think of a lower motor neurone lesion and reinforced our initial suspicion of a peripheral neuropathy. ACES for PACES page 443
Tone was difficult to examine in this patient as he kept tightening up his limbs.
Muscle power was decreased especially in the distal muscles again in keeping with a lower motor neurone lesion and peripheral neuropathy (ACES for PACES page 452)
Reflexes were diminished even with reinforcement again in keeping with our initial suspicion (ACES for PACES page 453)
Coordination was difficult to assess as the patient had weakness of his lower limbs
Sensation was diminished especially in the lower part of his limbs (stocking distribution) again in keeping with our initial suspicion (ACES for PACES page 455)
The diagnosis of a peripheral neuropathy had been made clinically the next step was to think about the causes of peripheral neuropathy
This was a distal symmetrical polyneuropathy which could be due to a number of causes (ACES for PACES page 434-435)

Differentiating Murmurs of Aortic Stenosis and Mitral Regurgitation

2008-12-12T04:50:00.000-08:00

One of the questions I was asked at the recent IBC Dubai PACES course was how would one differentiate the systolic murmurs of aortic stenosis from mitral regurgitation.
This is a good question. Most often it is very easy to make out whether it is aortic stenosis or mitral regurgitation but sometimes the features are not clear and then the differentiation can become exceedingly difficult.
The answer is not to depend on the characteristics of the murmur but to take into account all the other information gleaned on clinical examination.
To start with mitral valve disease is more likely in a female and aortic stenosis if the patient is a male (these are genralisations and not to be regarded as rules).
On general examination one may note a very pale appearance in association with aortic stenosis (Dresden doll appearance ACES for PACES page 180)
Elfin facies is associated with aortic stenosis ACES for PACES page 182
A malar flush would be in keeping with mitral valve disease and pulmonary hypertension ACES for PACES page 186
High arched palate may occur in supravalvular aortic stenosis ACES for PACES page 187
Atrial fibrillation more likely mitral valve disease ACES for PACES page 193
Low volume, slow rising pulse in aortic stenosis ACES for PACES page 193,194
Brachio-radial delay aortic stenosis ACES for PACES page 196
Displaced apex beat mitral regurgitation ACES for PACES page 202
Thrusting apex mitral regurgitation ACES for PACES page 202
Heaving apex aortic stenosis ACES for PACES page 202
Apical thrill mitral regurgitation ACES for PACES page 203
Thrill 2nd right intercostal space aortic stenosis ACES for PACES page 203
Soft 1st heart sound mitral regurgitation ACES for PACES page 205
Soft 2nd heart sound aortic stenosis ACES for PACES page 206
Pan systolic murmur radiating to the axilla inferior angle of scapula mitral regurgitation ACES for PACES page 211,213 (remember mitral regurgitation can also cause ejection systolic murmurs ACES for PACES page 211)
Ejection systolic murmur radiating to the neck aortic stenosis ACES for PACES page 210,213

This exercise in differentiating murmurs is a good illustration of the importance of following each step of the clinical examination, focussing one’s mind on the findings and analysing the findings before moving on to the next step (i.e. following the elephant’s footstep ACES for PACES preface)

History Taking, Communication and Ethics for MRCP PACES

2008-12-05T03:59:00.000-08:00

Many candidates and unfortunately many from outside the UK do not do well in these two stations.
One of the main reasons for this is failure to ask and take into account the patient’s, or in the case of a scenario in the communication skill station, the relation or carer’s perspective.
This may be due to the fact that this has not been standard teaching or standard practice when taking histories. Indeed many clinical skills books do not give a structure or framework for asking about the patient’s perspective.
It is essential to include the patient’s perspective in standard history taking. This is the only way in which one will do this naturally rather than in an artificial way in exams.
In order to do so it is vital to have a structure of framework for doing so.
In ACES for PACES I have provided such a structure (see chapters 4 and 18)
I have also provided an acronym as an aid to memorising this structure
It is I PASSED By Employing ACES, which stands for :
Identification and Introduction
Purposefully
Analyse
Symptoms
Systems
Elicit
Details
Beliefs
Expectations
Anxieties (regarding)
Causes
Effects
Survival

Cardiovascular Examination

2008-11-23T11:51:00.001-08:00

We had another good case at the recently concluded MRCP PACES course conducted by IBC in Dubai.
The patient was a young child who looked small.
In a small child with a cardiovascular problem one should consider congenital heart disease or rheumatic heart disease (ACES for PACES page 178)
On examination of the pulse we noted sinus rhythm approximately 80 beats per minute, no abnormality in volume or character, all pulses equal and synchronous.
No abnormality in the head or neck.
On examination of the praecordium the apex appeared displaced and was thrusting in nature.
A thrusting apex suggests mitral regurgitation, aortic regurgitation or ventricular septal defect (ACES for PACES page 202)
The fact that the pulse was of normal volume and not collapsing would make aortic regurgitation unlikely.
The fact that the pulse was in sinus rhythm would make mitral valve disease unlikely.
As we were already suspecting congenital heart disease VSD would be very likely.
On further palpation of the praecordium, we felt a systolic thrill at the left sternal edge. This would fit in with our suspicion of VSD.
Auscultation confirmed a harsh pan systolic murmur at the left sternal edge with no radiation of the murmur confirming our diagnosis of VSD.
Lungs were clear
Diagnosis
Ventricular Septal Defect
Sinus rhythm
No heart failure
No reversal of shunt

Respiratory Examination

2008-11-10T00:05:00.000-08:00

We saw another good case at the Dubai MRCP PACES course run by IBC.
The patient was a young Asian male man who seemed of normal height and weight.
On examination of his head there was no abnormality. On examination of his hands, initial examination seemed to reveal no abnormality, but on using the method of dividing the hands into systems (see ACES for PACES) it became evident that there was a difference in size and shape of the two hands. The left hand was smaller and narrower than the right. This was a consequence of an earlier injury during childhood. It had no bearing on the diagnosis but it did reveal the importance of correct method in revealing clinical findings.
On examination of the neck we noted that the trachea was deviated to the left. This indicated either a lesion pulling from the left or pushing it from the right.
On examination of the chest we noted that there was asymmetry of the chest with some flattening of the right apex and we also noted reduced movement of the right hemithorax. This showed that the lesion was on the right hand side. A lesion pushing the trachea from the right side. As a pneumothorax was unlikely in the setting of a course, the most likely diagnosis was right sided pleural effusion.
The remainder of the examination was now much easier as it was only confirmation of the findings of right sided pleural effusion.
The findings were an increased respiratory rate, apex beat was difficult to palpate, decreased vocal fremitus and reduced respiratory movements confirmed by palpation. Stony dull percussion note at the right base and decreased breath sounds and vocal resonance. Aegophony was heard at the upper border of the effusion.
Diagnosis
Right sided pleural effusion
Probably due to tuberculosis
Impaired respiratory function

Cardiovascular examination

2008-11-08T23:44:00.000-08:00

We saw a classic case at the recent Dubai PACES course conducted by IBC
The patient was a young man who looked fit and healthy.
His pulse rate was 80 beats per minute, regular rhythm. His JVP was not elevated, trachea midline. Apex was not displaced and normal in character. The first heart sound was loud. This was the first clue that there could be a valvular lesion and quite correctly the candidates thought that the patient may have mitral stenosis. The second hear sound was of normal intensity, suggesting that the patient had not developed pulmonary hypertension. There was a clear cut opening snap in keeping with mitral stenosis. There was the classic decrescendo mid-diastolic rumble heard just medial to the apex beat and there was pre-systolic accentuation of the murmur indicating vigorous left atrial contraction. The findings were accentuated by turning the patient to the left lateral position and by exercise.
Lungs were clear

Diagnosis
Mitral stenosis
Sinus rhythm
No heart failure or pulmonary hypertension
Most likely as a consequence of rheumatic fever

Cardiovascular Examination for MRCP PACES

2007-10-14T08:52:00.000-07:00

We had a doctor from another hospital attending PACES teaching for a few days. We wanted to show him how to approach a case in the exam and went through cardiovascular examination with him.
He started off as usual with a general examination and noted that the patient was seated up in bed, appeared breathless and had an oxygen mask on.
I asked him what he thought at this point, keeping in mind it was a patient with a known cardiovascular problem. He replied that he would say the patient had heart failure. (ACES for PACES page 177)
We asked him to carry on and he said he thought the patient was of average height and weight.
He next examined the patient’s hands. He went though in order and noted that the nails were normal, there were a few bruises on the skin, the bones, joints and tendons were normal but there was generalised wasting of the small muscles of both hands. I asked him why he thought the muscles were wasted and then he took a further look at the patient and said that he thought this was due to generalised wasting of muscles and that the patient looked emaciated. I asked him why the patient was emaciated reminding him that this was a patient with known cardiovascular disease. He replied that the most likely condition in the context of cardiovascular disease and heart failure was cardiac cachexia. (ACES for PACES page 179)
He next examined the pulse and said that the patient had a low volume pulse with several ectopic beats. I asked him what he thought the diagnosis was in a male patient in sinus rhythm (few ectopics) and a small volume pulse in a PACES simulation. (ACES for PACES page 190-195) He replied that the most likely diagnosis would be aortic stenosis. I reminded him that a diagnosis had more than one component and he then replied that the patient had aortic stenosis, was in heart failure and had cardiac cachexia.
On examination of the head the only abnormalities were flaring of the alae nasi in keeping with heart failure and a high arched palate.
On examination of the neck the JVP was not elevated and there were no other abnormalities.
On examination of the chest he noted a diffuse apex, soft 2nd heart sound and an ejection systolic murmur at the aortic area with radiation to the neck (ACES for PACES page 216-217)
There were basal crepitations.
We went through the findings again and reiterated how the diagnosis was made by the time he had finished examining the hands and that the remainder of the examination merely confirmed the suspicions that had been raised.

Respiratory Case

2007-09-30T10:40:00.000-07:00

I took some medical students to examine a patient.
The patient was an elderly man. He was seated up in bed and had an oxygen mask on. He was of average height but he looked thin. His skin was pigmented.
We paused there and analysed the findings up to that point. We thought that at this point we could think that the patient had a problem involving the respiratory system because of the breathlessness and it was probably a chronic illness because of the emaciation (ACES for PACES page 248).
We thought about the causes of skin pigmentation and thought of Addison’s disease in association with tuberculosis and we also thought about non-metastatic manifestations of bronchial carcinoma (ACES for PACES page 249)
On examination of the head we noticed that the head was thin and almost skeletal reinforcing our impression of emaciation and chronic illness.
The alae nasi were flaring reinforcing our impression that the patient was in respiratory distress.
There was no specific abnormality noted on examination of the hands.
On examination of the neck we noted that the neck was quite thin in keeping with the emaciation that we had noted.
The trachea was deviated to the left hand side.
The medical students went through the causes of tracheal deviation (ACES for PACES page 257)
Next, we examined the patient’s chest.
We noted that the patient’s chest wall was thin and almost skeletal. We also noted gynaecomastia. The medical students were asked why the patient was likely to have gynaecomastia in the context of the other findings so far. Non-metastatic manifestations of bronchial cancer came to mind (ACES for PACES page 259)
The respiratory rate was 28 per minute
Respiratory movements were decreased on the right hand side. We stopped there and asked the students what the causes of decreased respiratory movements were (ACES for PACES page 261)
We then asked in the context of the findings so far what the diagnosis could be
Tracheal deviation to the left and reduced movements on the right would suggest either pleura effusion or pneumothorax on the right side. However we had already thought that the illness was a chronic process and this made us think that the diagnosis was pleural effusion
Taking into account the emaciation, pigmentation and gynaecomastia the cause of the effusion was most likely a bronchial cancer.
Vocal fremitus was decreased on the right hand side in keeping with our suspicion of pleural effusion on that side. (ACES for PACES page 262)
Percussion note was stony dull on that side in keeping with pleural effusion (ACES for PACES page 262)
Breath sounds were decreased on the right hand side vocal resonance was reduced and there was aegophony at the upper level of the effusion (ACES for PACES page 263-264)
Diagnosis
Right sided pleural effusion underlying bronchial cancer

Cardiovascular Examination for MRCP PACES

2007-08-08T22:46:00.000-07:00

We saw an interesting case today.
The trainee examined the patient and presented the findings and following this we went through the technique of cardiovascular examination in detail and analysed the findings.
We started off by having a general look at the patient and her surroundings. There was a yellow booklet by the bedside, which indicated that the patient was on warfarin. This immediately made us think of either an arrhythmia such as atrial fibrillation or a metallic heart valve.
The patient was a young female who was seated comfortably in bed. She was of average height but slim. Her skin was deeply tanned. I asked the trainee what the tan would mean and we concluded that this meant the patient was not unduly unwell and had been fit enough to go on holiday.
There was no marked abnormality on examination of the head although her palate seemed high arched.
There was no abnormality of her hands; her pulse rate was 80 beats per minute and regular, normal volume and character, no radio-radial or radio-femoral delay.
The fact that she was in sinus rhythm made us think she was on warfarin for a prosthetic valve.
There was no abnormality of her neck. In particular the JVP was not raised and the trachea was in the midline.
On examination of her chest a midline sternotomy scar was noted. The presence of the scar together with the fact that we had already noted the anticoagulation booklet made us think the patient had a prosthetic heart valve reinforcing the impression we had made by noting that she was in sinus rhythm.
The apex beat was in the 5th intercostal space just medial to the midclavicular line and the character was normal.
The heart rate was also 80 beats per minute and regular, dual rhythm.
The first heart sound was normal.
The second heart sound was replaced by a closing click of a prosthetic valve. This made us think that she had a prosthetic aortic valve. We listened carefully in systole and heard an opening click at the left sternal edge. Further evidence that she had a prosthetic aortic valve.
There was a soft systolic murmur at the aortic area, which was not conducted to the neck. Probably a flow murmur. No diastolic murmur was heard. No extra-cardiac sounds were heard.
There was no oedema and the lung bases were clear. However when we examined the patient’s back we noted a left sided thoracotomy scar
The trainee concluded that the patient had a prosthetic aortic valve, she was in sinus rhythm and that there was no evidence o heart failure. There was no valvular leak.
I asked him what the thoracotomy scar could be due to. One of our previous trainees who is now a registrar had a similar case when he went for the PACES examination and had been stumped by this question. The answer was easy for us and we were able to confirm that she had an earlier operation for repair of coarctation of the aorta.
I did include this in ACES for PACES page 201 so that candidates preparing for the MRCP PACES would be aware of such a possibility. The late complications of coarctation of the aorta include aortic valve disease because of associated bicuspid aortic valve.
One of the signs the trainee missed was the opening click. I know that this is one of the features that examiners at the PACES often question the candidates on and hence it is important not to miss it.
We went thorough the method of auscultation of the heart and reinforced the importance of heaving a robust method and sticking to it. Placing one’s stethoscope over the praecordium and listening to what one may hear is not enough. One must go through each phase of the cardiac cycle and analyse each component. (See ACES for PACES pages 165-169 summarised on page 170)
Another important point illustrated by the presentation of this case is the importance of a complete diagnosis. Replaced aortic valve, no leak, sinus rhythm, no heart failure, aetiology bicuspid aortic valve associated with coarctation of the aorta.
In other words the four components of diagnosis (ACES for PACES chapter 3)

MRCP (UK) Part 2 Clinical Examination (PACES) and Clinical Guidelines

2007-08-04T08:33:00.001-07:00

I spoke to a doctor who had failed the MRCP PACES on two occasions. I questioned him at length on how he had prepared for the examination. I next showed him the booklet produced by the Royal College of Physicians of Edinburgh, London and Glasgow. He had never seen it before and did not know that such a publication existed.
We went through some of the sections and I pointed out what the colleges were expecting from the candidates. He was completely unaware of what was expected and had approached preparation in the wrong way.
The booklet clearly states what knowledge and skills are expected of the candidates at each station and then gives the mark sheets so that one may get an idea of how marks are awarded.
It is surprising that many candidates are unaware of the existence of such a publication and hence their preparation is misdirected and incorrect.
I would recommend that those who are taking the exam should go through this booklet and use this to guide their preparation.

Presenting the Diagnosis in MRCP PACES

2007-07-29T02:45:00.000-07:00

I spoke to a candidate who had failed the MRCP PACES at his last attempt. We discussed presentation of findings to the examiners and in particular how to present one’s diagnosis.
I asked him how he had presented the diagnosis of the cases he had seen at the examination and the information he gave me was inadequate. He gave basic information but left out very important facts concerning function of the system concerned and aetiology.
This led us to discuss diagnosis in detail.
I realised that this candidate had not analysed what is meant by diagnosis and had not studied this in depth.
When coming to a diagnosis it is important to make this as complete as possible and find out about the organ or system concerned, the pathology affecting the organ or system, the aetiology of the illness and the function of the organ or system
In other words it is important to elucidate the four components of a diagnosis:
Anatomical diagnosis (where is the lesion)
Pathological diagnosis (what is the pathological process)
Aetiological diagnosis (what is the cause of the lesion)
Physiological diagnosis (what is the function of the organ or system concerned)
If one presents one’s diagnosis in this manner it will demonstrate to the examiner that one is thinking clearly and this is likely to influence the marks obtained.
For an analysis of diagnosis, the four components of diagnosis and checklists for use in situations where it is difficult to come to a diagnosis; see chapter 3 of ACES for PACES

MRCP PACES Respiratory Station

2007-07-22T14:06:00.000-07:00

I spoke to a candidate who failed the MRCP PACES. We discussed the case he had at the respiratory station.
He had a case of fibrosing alveolitis (interstitial lung disease). He said he easily made the diagnosis and knew everything about fibrosing alveolitis and was waiting for the examiners to ask him about fibrosing alveolitis so he could display his knowledge.
Unfortunately for him this was the MRCP PACES and what was being assessed was demonstration of practical examination and evaluation skills not, encyclopaedic knowledge of theory.
He was asked how he would demonstrate clubbing (see ACES for PACES pages 107,126) and he was then asked about the causes of clubbing (see ACES for PACES pages 126,254)
He was also asked about cyanosis and the types of cyanosis (see ACES for PACES page 116)
He made crucial mistakes in these basics and did not satisfy the examiners.
This is quite a common error. Many candidates prepare for PACES by studying all the details of likely cases rather than going through the basics. The examiners are looking to see if the candidate demonstrates ability to examine a patient correctly and then interpret the signs obtained.
Theory knowledge has already been assessed in parts 1 and 2 and will not be assessed here.

Fail MRCP PACES physical examination stations

2007-07-15T13:56:00.000-07:00

I had discussions with several examiners for the MRCP PACES. I asked them how they would decide on passing or failing a candidate at the physical examination stations.
They all said the first thing they look at is how well the candidate examines the patient. If the candidate does not demonstrate correct technique or if they do not examine with ease then they would fail the candidate.
If the candidate passes this first hurdle the next step is whether they detect the physical signs present. With regard to physical signs they would not mind if a difficult sign was missed but they all said they would definitely fail the candidate if they “ made up physical signs”. That is if the candidate tells the examiner that the patient has a physical sign that is not there then, the examiners will definitely fail them. I asked several candidates how they prepare for the exam and they said they memorise the physical signs of the likely cases in the exam.
This technique of exam preparation is incorrect.
This is the reason why a lot of candidates fail the exam despite examining correctly and making the correct diagnosis. Memorising the physical signs and repeating this at the exam instead of telling the examiners the findings that are present in the case in question is why most candidates fail.
So in summary the main reasons for failing the MRCP PACES physical examination stations are:
1) Incorrect technique
2) Making up physical signs

Pass MRCP PACES

2007-06-23T01:55:00.000-07:00

I spoke to two MRCP PACES examiners last week. One was a senior examiner who had been involved in the PACES exam since its inception and the other was one who examined for the first time this diet. Both had the same views when it came to marking candidates.
They stressed that what was most important was correct method. They observed the candidates going through history taking, clinical examination and communication and noted whether they appeared competent in the skill they were demonstrating. If they demonstrated competence they were most likely to pass.
If the candidate failed to demonstrate competence at history taking, clinical examination and communication then they would fail even if they got the findings right.
One of the examiners gave me two examples of candidates who examined the abdomen and the respiratory system. Both had what he described as appalling technique but both were able to give all the findings when asked. However, both failed, as the exam is a judge of the ability of the candidate to demonstrate or show competence in clinical method rather than an ability to memorise the findings in a given condition.
The secret of passing the PACES examination is practising clinical methods (history taking, physical examination and communication) over and over again until you can do it without even thinking about what comes next. Then you will pass with ease

History Taking, Communication and Ethics for MRCP PACES

2007-06-02T00:50:00.000-07:00

We had a discussion regarding these two stations. Every medical student begins learning clinical skills by learning how to take a history. By the time a doctor takes the MRCP PACES examination these skills should be second nature to him or her. Then why are so many failing in this station?
We discussed this further using examples of scenarios.
The first thing to remember is that most of the stations involve simulated patients or relatives. They have been told what to say regarding a certain condition or situation. If one asks a question they will answer according to the instructions given. If they are not sure, they will give you the answer rather than risk hiding an important fact and prejudicing the candidate’s chances.
What are the questions one should ask?
The questions to be asked in history taking are standard and these should not present a problem. (Presenting complaint, past illnesses, drug history etc)
The questions that one should ask to make the history more relevant and display maturity on the part of the clinician are the extra questions that are not yet considered standard.
These questions are regarding the beliefs, expectations, anxieties or concerns of the patient. If they are not asked very important information is missed out and this is usually the cause of failure especially in the communications and ethics station.
If one does not take into account the thoughts and views of the patient or the concerned party, then the explanation will lack focus on the situation in and will simply be a general explanation which may not suffice in that particular situation.
To make sure that you take into account these additional parts of the history, use the mnemonic:
I PASSED By Employing ACES (see ACES for PACES chapter 4, chapter 18)
The second part of these stations is delivering an explanation to the patient or concerned party regarding the situation. This explanation is best given by telling them in simple language what one’s own beliefs, expectations and concerns are regarding the situation (ACES for PACES chapter 18)
By having such a framework for assessing and explaining, the whole process becomes methodical and thus simplified.
We went through several scenarios using this method.
A scenario concerning a pregnant woman who has a deep vein thrombosis; the concern of the patient is that the treatment will cause harm to the foetus. If this concern is not elicited and addressed the explanation would be deemed unsatisfactory.
Similarly, a patient with a stroke and the scenario is regarding feeding, the relation may be concerned that not feeding and starving the patient may cause distress or on the other hand the concern may be that feeding would prolong the patient’s suffering. Hence it is important to elicit these thought and views and address these anxieties.

Cardiovascular Examination for MRCP PACES

2007-05-27T22:00:00.000-07:00

The trainee was asked to examine the patient's cardiovascular system. He carried out the examination and he was then asked to present his findings.
The presentation was as follows:
The patient is an elderly gentleman who is of average height and weight. There are no signs of bacterial endocarditis. Pulse 80 beats per minute regular, no collapse.
No cyanosis.
JVP not elevated
Apex 5th left intercostal space, medial to the mid-clavicular line
First heart sound was soft. There was a pan systolic murmur best heard at the apex with radiation to the axilla. The murmur increased in intensity during expiration.
He was then asked the diagnosis and replied that the patient had mitral regurgitation.
We then thought we would go through the patient again. This time we went more slowly, following the method (ACES for PACES pages 157-171), we meticulously went though each step and analysed one step at a time
We started with a general examination.
The patient was an elderly gentleman of average height and weight. He was lying propped up in bed and appeared tachypnoeic. We paused to think what this would indicate and decided that on this information and the fact that we were examining the cardiovascular system, the patient must have heart failure.
We looked at his head, quickly went though the general examination and then looked at his nose. His alae nasi were flaring; in keeping with the suspicion that the patient had heart failure.
On examination of his mouth we noticed that the patient had a high arched palate.
On examination of his hands, there was no abnormality of his nails but on examination of the skin we noted multiple bruises. In the context of the cardiovascular system this could indicate that the patient was being treated with an anticoagulant.
His pulse rate was 80 beats per minute, regular in rhythm and volume no collapse, normal character, no radio-radial, radio-femoral or brachio-radial delay.
We asked the patient to stretch his palms out, there was no tremor. We asked him to spread his finger wide apart and cock his wrists back and noted that the patient had a flapping tremor. We thought about the causes of a flapping tremor and decided that of the many causes pf a flapping tremor; this patent’s tremor was most likely to be due to heart failure (see ACES for PACES page 446 causes of flapping tremor)
On examination of his neck there were no abnormalities on general examination, no goitre, muscles normal. His JVP was elevated to his ear lobe. The trainee remarked that he had noted the pulsation in the patient's neck but thought that this was carotid pulsation. We then went through how to differentiate pulsations in the neck (see ACES for PACES page 162)
The predominant wave in the JVP was a systolic wave, which was expansile, a V wave, and this suggested that the patient had tricuspid regurgitation.
The carotids were normal; the trachea was in the midline.
There was no structural abnormality of his praecordium, skin was normal and there were no visible pulsations.
The apex beat was in the 5th left intercostal space just medial to the mid-clavicular line and it was diffuse in nature. There was no left parasternal heave.
The heart sounds were regular in rhythm 80 beats per minute. The 1st heart sound was soft. This made us think that the patient had mitral regurgitation.
The 2nd heart sound was normal in intensity and not split.
There was a pan systolic murmur at the apex and this murmur radiated to the axilla. The murmur increased in expiration. This was in keeping with the earlier suspicion that the patient had mitral regurgitation.
There was a pan systolic murmur at the left sternal edge. It was difficult to say whether this murmur increased in inspiration. The murmurs were in keeping with mitral and tricuspid regurgitation, which we suspected from our earlier findings.
On examination of the back we looked at the neck and spine and traced our fingers down the spine as recommended in the method and this enabled us to readily observe that the patient had sacral oedema, in keeping with our suspicion that the patient had heart failure.
On auscultation of the lung bases we noted that the patient had fine bilateral basal crepitations. Further evidence in favour of our suspicion that the patient had heart failure.
Diagnosis:
Mitral and tricuspid regurgitation
Sinus rhythm
Congestive cardiac failure
We discussed the differences in the amount of information obtained and came to the conclusion that following the method and concentrating on one step at a time enabled us to obtain much more information.
The recommendation to the trainee was to read the method over and over again and practice over and over again until the method became second nature to him. Read, practice, read again ad infinutm.
Further questions:
What is the cause of the mitral regurgitation? (See causes of mitral regurgitation ACES for PACES page)
Advanced level question:
Is it primary valvular disease or regurgitation secondary to cardiac dilatation?
The absence of a loud 2nd heart sound makes it unlikely that the patient has developed pulmonary hypertension and further the absence of left parasternal heave makes it unlikely that that patient had developed right heart failure secondary to chronic left heart failure and pulmonary hypertension.
Hence, the valvular regurgitation was more likely to be due to heart failure and cardiac dilatation.
Notes on mitral regurgitation :
http://www.medicalrevision.org/mitral_regurgitation.htm

Cardiovascular Examination MRCP PACES

2007-04-21T00:49:00.000-07:00

The patient was a middle aged female. She was propped up in bed and breathless. We asked the trainee what her thoughts were and she replied that in the context of a cardiovascular examination, breathlessness would suggest the patient had heart failure.
She was of average height and weight.
On examination of her head, the only abnormality seen was flaring of the alae nasi in keeping with the impression that the patient was in heart failure.
On examination of her hands there was no abnormality.
Her pulse rate was 90 beats per minute regular in rhythm and volume. The pulse was large in volume and collapsing in nature. This was a definite collapse and a good example. We went through the technique of demonstrating a collapsing pulse (ACES for PACES page 159) We discussed the causes of a collapsing pulse (ACES for PACES page 194) and the trainee concluded that in the context of the PACES examination, a collapsing pulse would most likely indicate aortic regurgitation.
There was no bisferiens pulse. This made mixed aortic valve disease less likely.
On examination of her neck it was noted that the jugular venous pressure was elevated about 5 cms above the manubriosternal angle. This was further evidence in favour of the impression that the patient had heart failure. In this patient a pulsation in the neck could also be exaggerated carotid pulsation , Corrigan’s sign ( ACES for PACES page 200 abnormalities of the carotid pulse)
Hence, it was important to differentiate between this and the jugular venous pulse. We went through how to analyse pulsations in the neck (ACES for PACES page 162)
The trachea was in the midline.
On examination of the chest it was noted that there were no deformities or pulsations of the praecordium. The apex beat was in the 6th left intercostal space in the anterior axillary line and it was thrusting in nature.
A displaced apex in the context of a trachea in the midline would suggest the heart was dilated (not mediastinal shift).
See ACES for PACES page 201-203 abnormalities of the apex beat
This was in keeping with the impression that the patient had aortic regurgitation.
The thrusting apex was also in favour of this diagnosis.
There was no parasternal heave and there were no thrills.
There was an ejection systolic murmur in the aortic area, which did not radiate and there was a decrescendo early diastolic murmur at the left sternal edge, which increased in intensity when the patient leaned forward and held her breath in expiration.
On auscultation of her lung bases bilateral basal crepitations were heard.
On auscultation over her femoral arteries a systolic bruit was heard.
Diagnosis:
Aortic regurgitation, sinus rhythm, heart failure
We went through the questions that could be asked in relation to this case.
First, what are the causes of aortic regurgitation and after that how does one assess severity (ACES for PACES page 216)
Next, how does one investigate the patient? (See planning investigation ACES for PACES pages 571-574)
How does one manage this patient? (See planning management ACES for PACES pages 574-577)
Notes on aortic regurgitation :
http://www.medicalrevision.org/regurgitation.htm

Respiratory Examination for MRCP PACES

2007-04-21T00:26:00.000-07:00

The patient was an elderly male resting comfortably in bed. He was of average height and weight.
On examination of his head the trainee noted that the patient had xanthelasma on his lower eyelids. She concluded that they were probably of no significance in relation to the patient’s respiratory problem.
On examination of his hands the trainee noted that the patient had clubbing (increased nail bed fluctuation, loss of the nail be angle, increased curvature of the long axis of the nail; stage 3 clubbing see ACES for PACES page 127). At this point we emphasised the importance of recalling the causes of clubbing with special reference to the causes in relation the respiratory system (see ACES for PACES pages 127,254).
There were no other abnormalities detectable on examination of the hands.
There were no abnormalities detected on examination of the neck. The trachea was in the midline.
On examination of the chest the trainee noted that the chest was normal in size and shape with normal respiration with equal movements of the two sides of the chest. The respiratory rate was 16 per minute; the apex beat was in the 5th left intercostal space just medial to the midclavicular line. Vocal fremitus was normal and equal on the two sides; respiratory movements by palpation were equal on the two sides. Percussion note was resonant and equal on the two sides. Breath sounds were vesicular. There were fine late inspiratory crepitations at both lung bases. This made the trainee consider the causes of fine crepitations at the lungs bases (see ACES for PACES page 264 –265). She thought of fibrosing alveolitis. In association with clubbing this was the most likely diagnosis. Vocal resonance was normal and equal on the two sides.
Diagnosis:
Fibrosing alveolitis, not in respiratory failure clinically
Next, we considered the questions that could be asked
First, we went through the causes of fibrosing alveolitis (ACES for PACES pages 239-240)
Next, we considered the investigations that one may arrange on this patient (see planning investigation ACES for PACES pages 571-574)
Finally, we considered management of the patient (see planning management ACES for PACES pages 574-577)

Neurology for MRCP PACES

2007-04-14T01:16:00.000-07:00

The patient was an elderly lady who was seated comfortably. She was of average height and weight
On examination of the upper limbs there was no major change in size or shape of the limbs; the skin was normal.
On examination of the muscles the trainee noticed that there was some wasting of the small muscles of the hand involving the thenar eminence bilaterally and the interossei. However, the wasting was not uniform. She also noted fasiculations in the triceps muscles.
At this point we interrupted and asked what her thoughts were. The reply was that with a combination of wasting and fasciculation the most likely diagnosis was motor neurone disease.
On examination of power, the trainee noted that there was weakness mostly distally (small muscles of the hand) the distribution of the weakness was not uniform. This added more weight to the initial suspicion that the patient had motor neurone disease.
Reflexes were exaggerated bilaterally and Hoffman’s sign was positive. Exaggerated reflexes were evidence that the upper motor neurones were involved and this suggested that the patient had amyotophic lateral sclerosis.
There were no overt cerebellar signs and there was no sensory deficit. This was further evidence in favour of motor neurone disease.
Diagnosis:
Amyotrophic lateral sclerosis
Revision Tips
Revise the degenerative disorders of the motor neurones ACES for PACES pages 439-440

MRCP PACES 2nd diet 2007

2007-04-14T01:15:00.001-07:00

We began teaching for the 2nd diet of the PACES. Only a few candidates this time as the majority passed last time
As usual teaching will concentrate on the basics, as this is what is needed to pass a clinical examination

Neurology for MRCP PACES

2007-02-21T22:47:00.000-08:00

The patient was an elderly man lying comfortably in bed. He was of average height and weight.
On examination of his upper limbs there were no abnormalities of size and shape of the limbs and the skin was normal. This excluded a neurological deficit dating back to childhood, (normal size and shape) and significant sensory deficit as there were no skin changes.
No wasting was apparent on routine inspection of the upper limbs and there were no involuntary movements.
Tone was normal at the wrist and the elbow but tone was flaccid at the shoulder. When the patient's arms were raised above the head and let go they fell away without any control. This showed that he had flaccidity at the shoulder and this raised the possibility of either a myopathy or lower motor neurone lesion at the shoulder (see ACES for PACES page 449)
The trainee examined power beginning at the shoulders and working distally and demonstrated weakness of abduction and adduction at the shoulder.
He was asked to re-examine power in the upper limbs beginning distally (starting with the small muscles of the hands) and working proximally (to the shoulders and the muscles around the scapula). This time he noticed that there was wasting of the muscles around the scapula and there was weakness of abduction and adduction at the shoulder and weakness of the muscles around the scapula. This suggested either a myopathy or a lower motor neurone lesion affecting C4, C5.
On examination of his reflexes the biceps jerk and triceps jerk were exaggerated there was an inverted supinator jerk and Hoffman's sign was positive. This indicated a lower motor neurone lesion at C5 with upper motor neurone lesion below that level (see ACES for PACES page 508). This together with the signs found earlier would indicate that he had a lower motor neurone lesion affecting C4, C5 with an upper motor neurone lesion below that level. This would fit in with a cervical myelopathy.
Coordination was poor but this reflected the proximal weakness rather than a cerebellar lesion
On examination of the sensory system there was loss of sensation over C4, C5 on the right hand side and equivocal loss of sensation over C4, C5 on the left hand side
Diagnosis
Cervical myelopathy affecting C4, C5 nerve roots
Learning points
This case was difficult for the trainees. The main reason for missing the diagnosis, in the first instance, was that there was a failure to follow the correct method.
Not examining tone at the shoulder was a crucial mistake. This would have shown evidence of flaccid weakness affecting C5
Examining power by beginning proximally was the most crucial error. The scapular region was not examined and this meant that the wasting and weakness around the scapula was missed and thereby crucial evidence was missed.
The trainee had not seen an inverted supinator jerk before but this is an important sign to look for when performing the tendon reflexes. An additional problem was that the Hoffman reflex was not elicited correctly and hence the positive reflex was missed. Practice performing the Hoffman reflex using the correct method (ACES for PACES page 414)
By the time the reflexes were examined the diagnosis was clear and sensory examination only added further evidence to confirm the earlier suspicions.
Remember the secret of success in neurology is following correct method and analysing at each step. Read up the section on examination of the CNS in chapter 16 of ACES for PACES and practice repeatedly.
Revision Tips
Revise the nerve supply of the skin, the muscles and the reflexes ACES for PACES pages 426-428

Cardiovascular Examination for MRCP PACES

2007-02-21T22:24:00.000-08:00

The patient was an elderly female lying propped up in bed. She was of average height and weight.
There were no abnormalities seen on examination of her head.
On examination of her hands there were no abnormalities found. Her pulse rate was 80 beats per minute, regular in rhythm and volume, normal character, all pulses were equal and synchronous.
On examination of her neck, the JVP was elevated to the angle of the jaw. The dominant wave was an expansile systolic wave. This made the trainee think of tricuspid regurgitation. The venous wave was under high pressure and palpable. This made the trainee think that the cause of the tricuspid regurgitation was right heart failure due to pulmonary hypertension. As the patient did not appear to have significant pulmonary disease the suspicion was that this was due to long standing left ventricular dysfunction.
The trachea was in the midline.
There were no abnormalities seen on inspection of the chest, the apex beat was palpable in the 6th left intercostal space lateral to the midclavicular line. This made the trainee think that either the patient had systolic heart failure or dilatation of the ventricle due to diastolic overload caused by valvular regurgitation. There was no thrust or heave at the apex and there was no parasternal heave.
The 1st heart sound was soft making the trainee think that the mitral valve was not competent. The second sound was also soft.
There was an opening snap heard best at the mitral area this made the trainee think that there was stenosis of the mitral valve.
There was an ejection systolic murmur radiating to the neck suggesting that the patient has aortic stenosis. There was a pan- systolic murmur at the left sternal edge and this increased with inspiration in keeping with tricuspid regurgitation. This had been suspected earlier on the basis of the characteristics of the JVP.
There was also a pan systolic murmur at the mitral area. This increased in expiration and radiated to the axilla in keeping with mitral regurgitation that had been suspected earlier on the basis of the soft 1st heart sound. There was a rumbling mid-diastolic murmur at the mitral area in keeping with mitral stenosis.
There was no sacral oedema and the lung bases were clear.
Diagnosis
Mitral stenosis
Mitral regurgitation
Aortic stenosis
Tricuspid regurgitation
Questions
How would you know whether the mitral stenosis or regurgitation was dominant?
In this case one would suspect that mitral regurgitation was dominant. The pulse was of normal volume, the apex beat was displaced and the first heart sound was soft (see table in ACES for PACES page 221)
How would you tell whether the aortic valve was severely narrowed?
The aortic stenosis was not severe in this patient because she had a normal volume pulse; there was no brachio-radial delay, no thrill, no fourth heart sound (see ACES for PACES page217)
Can a mid-diastolic murmur occur in mitral regurgitation?
Yes, severe mitral regurgitation can cause a flow murmur in mid-diastole (see causes of mid-diastolic murmurs ACES for PACES page211-212)
How do you know that this is not a flow murmur?
The patient has an opening snap, which would suggest stenosis of the mitral valve
Revision Tips
Revise auscultation of the heart ACES for PACES pages 204-222

Neurology for MRCP PACES

2007-02-15T22:24:00.000-08:00

The patient was a young man lying comfortably in bed
He was of average height and weight
On examination of the lower limbs the trainee noted that there was no major change in the overall size of the limbs and there were no trophic changes in the skin. These findings indicated that the lesion was not long standing.
The muscles of the lower limb were wasted; there were no involuntary movements. This suggested that the lesion affected the lower motor neurone. The absence of involuntary movement, in particular fasiculations, suggested that the anterior horn cell was not affected.
Tone was flaccid reinforcing the idea that this was a lower motor neurone lesion.
Power was decreased throughout the lower limb with the distal muscles being affected to a greater degree. In keeping with a lower motor neurone lesion. The distribution of the weakness was a paraparesis. What we had now demonstrated was a flaccid paraparesis. This narrowed the possibilities down to just a few (ACES for PACES page 452). Of these options, flaccidity narrowed the possibilities down even further leaving us with the possibility of either a radiculopathy or cauda equina lesion.
Reflexes were absent even with reinforcement, further evidence in favour of a lower motor neurone lesion. Eliciting reinforcement allowed us to see that the upper limbs were functioning normally reinforcing our idea that this was a paraparesis.
It was not possible to test coordination in the lower limbs in view of the weakness.
Sensory examination did not reveal a gross deficit; there was equivocal loss of light touch over the feet. This would be a feature against a cauda equina lesion, as the patient would have had anaesthesia in a saddle distribution.
The most likely diagnosis was a polyradiculoneuropathy.
The candidate was asked whether he would like to ask the patient a question regarding the condition to reinforce the diagnosis. The question was whether the patient’s bladder or bowels were affected. Although autonomic features are common in acute inflammatory demyelinating polyradiculoneuropathy (Guillain-Barre syndrome, AIDP) the bladder is not commonly affected whereas it is commonly affected in cauda equina lesions.
The candidate was also asked whether there was any other physical examination he would like to conduct to exclude a cauda equina lesion. The answer was per rectal examination and testing for anal tone, which would be reduced, and the anal reflex, which would be absent in cauda equina lesions.
Diagnosis
Flaccid paraparesis due to a polyradiculoneuropathy possibly acute inflammatory demyelinating (the onset was over a short duration) or Gullain- Barre syndrome
Revision Tips
Neurology is a difficult subject and is often considered daunting by most candidates attempting the PACES examination.
It is helpful to know the causes of the types of deficit that occur in neurological practice as this will enable one to localise the site of the lesion
Study the causes of wasting of muscles (ACES for PACES page 443)
Study the causes of flaccidity (ACES for PACES page 449)
Study the different types of distribution of muscle weakness (ACES for PACES page 451-453)
Study the patterns of sensory loss and their causes (ACES for PACES page 455-456)

Cardiovascular examination for MRCP PACES

2007-02-03T02:34:00.000-08:00

The patient was a middle-aged man who was propped up in bed. He had an oxygen mask on. The fact that he appeared breathless made the trainees suspect that the patient may have left ventricular failure. He was of average height and weight.
On examination of his head he had flaring of his alae nasi, which gave the trainees further evidence of dyspnoea.
On examination of his hands there was clubbing which immediately brought up the suspicion of infective endocarditis.
His pulse rate was 90 beats per minute regular in rhythm. It was a large volume pulse and it was collapsing in nature. Sinus rhythm with a collapsing pulse made the trainee suspect that the patient had aortic regurgitation. Careful examination of the character of the brachial pulse revealed a Bisferiens pulse. This brought up the diagnosis of mixed aortic valve disease.
On examination of the neck the jugular venous pressure was elevated. the predominant wave was a systolic wave causing outward distension of the vein. The trainee though this was a V wave indicating tricuspid regurgitation. The trachea was in the midline.
On examination of the praecordium, the apex was palpable in the 6th intercostal space in the anterior axillary line. It was diffuse in nature. With the trachea in the midline the apex being palpable in the 6th intercostal space in the anterior axillary line indicated dilatation of the heart rather than mediastinal displacement. This would be in keeping with the suspicion of aortic regurgitation although it was not thrusting in nature.
On auscultation the first heart sound was soft suggesting mitral regurgitation.
The second heart sound was soft in keeping with aortic stenosis.
There was an ejection systolic murmur radiating to the neck and a blowing, decrescendo early diastolic murmur at the left sternal edge. Confirming our suspicion of mixed aortic valve disease. There was a blowing pan-systolic murmur at the mitral area that increased in intensity during expiration adding further evidence to the earlier suspicion that the patient had mitral valve disease (tricuspid regurgitation would have made the murmur increase in inspiration)
On auscultation of the ling bases there were fine late inspiratory crepitations in keeping with the earlier suspicion that the patient had left ventricular failure.
The trainee was then asked to listen over the femoral artery.
There was a systolic and diastolic bruit over the femoral artery, which confirmed the suspicion that the patient had aortic regurgitation.
Diagnosis
Mixed aortic valve disease (dominant regurgitation)
Mitral regurgitation
Tricuspid regurgitation
Possible infective endocarditis
Revision Tips
Revise character of the pulse (ACES for PACES page 194)
Revise differentiation of mixed valve disease (ACES for PACES pages 220-221)
Revise abnormalities of the femoral artery (ACES for PACES pages 223-224)

Abdominal examination for MRCP PACES

2007-02-03T00:08:00.000-08:00

The patient was a middle-aged man lying comfortably in bed. He was of average height. His weight was difficult to judge as his abdomen was distended but there appeared to be loss of weight as his extremities looked thin.
On examination of his head his sclerae were icteric making the trainee immediately suspect that the patient had liver disease. There were multiple telangiectasia over his face in keeping with hepatocellular failure. There was bilateral parotid enlargement which made the trainee suspect that the aetiology of the condition was alcohol abuse.
On examination of the hands there was palmar erythema another feature of hepatocellular failure. He had Dupuytren’s contracture, which was another feature that would suggest the aetiology of the condition was alcohol abuse.
He had multiple spider naevi over his upper chest a further indication of hepatocellular failure. There was no gynaecomastia and the distribution of hair growth over his chest was normal.
The abdomen was distended and the distension was greatest in the flanks this made the trainee suspect that the patient had ascites. There were visible veins on the anterior abdominal wall and the direction of blood flow was from caudal to cranial. This suggested that the patient had portal hypertension.
On palpation of the abdomen no lumps or organomegaly were detected. Percussion demonstrated a horseshoe shaped area of dullness and shifting dullness confirming the trainee’s earlier suspicion that the patient had ascites. Auscultation did not reveal any abnormality.
At this point the trainee was asked to employ the technique of “dipping” and with this technique she was able to note that the liver was enlarged three finger breadths below the costal margin but the enlargement was not detected by routine palpation because of the presence of ascites. This was an important learning point. In the presence of ascites always employ “dipping” to detect organomegaly or masses.
Diagnosis:
Features of chronic hepatocellular failure
Features of portal hypertension
Hence clinical diagnosis of cirrhosis of the liver
Aetiology probably alcohol abuse
Revision Tips
Learn the clinical features of cirrhosis of the liver (the features of hepatocellular failure, features of portal hypertension) the causes of cirrhosis of the liver and clinical clues to the causes of cirrhosis of the liver (ACES for PACES pages 305-306)
Learn the technique of “dipping” (ACES for PACES page 273)

Cardiovascular case for MRCP PACES

2007-02-02T23:19:00.000-08:00

The patient was an elderly female. She was lying propped up in bed and had an oxygen mask on. The trainees were asked what their impression was at that point.
Breathlessness in a patient with a cardiovascular problem was most likely to be due to left ventricular failure.
The patient was of average height but appeared to be thin. The trainee said that this probably indicated that the patient was cachectic on account of chronic illness.
On examination of the head the only physical sign of note was that the patient had flaring of the alae nasi in keeping with the suspicion of left ventricular failure.
On examination of the hands the trainee noted clubbing. In the context of the cardiovascular system there are few causes of clubbing. In the absence of cyanosis and in an elderly patient who was unlikely to have congenital heart disease (even after operative correction) the chances were the patient had infective endocarditis. There were no other peripheral stigmata of infective endocarditis.
The pulse rate was 80 beats per minute irregular in rhythm and volume indicating atrial fibrillation. Atrial fibrillation made the trainee suspect that the patient was likely to have mitral valve disease.
On examination of the neck it was noted that the jugular venous pressure was elevated and it was predominantly a systolic wave, which resulted in outward distension of the vein. This made the trainee think it was a V wave due to tricuspid regurgitation. A V wave in the context of atrial fibrillation and suspected mitral valve disease would raise the suspicion that the patient had right ventricular involvement secondary to the development of pulmonary hypertension as a consequence of mitral valve disease.
On examination of the praecordium it was noted that there was a midline sternotomy scar. This raised the possibility of valve replacement or bypass grafting.
The apex beat was displaced to the 6th intercostal space in the anterior axillary line. It was thrusting in nature. This would indicate that the left ventricle was dilated and there was diastolic overload. With the suspicion of mitral valve disease already raised on account of atrial fibrillation the most likely diagnosis at the moment was mitral regurgitation.
There was left parasternal heave and a palpable pulmonary second sound best felt at the pulmonary area. This was in keeping with the earlier suspicion that the patient had developed pulmonary hypertension as a consequence of mitral valve disease.
On auscultation of the heart the native first heart sound was replaced by a click indicating a prosthetic mitral valve.
The second heart sound was complicated. At the pulmonary area a loud native heart sound was heard in keeping with pulmonary hypertension. At the left sternal edge a click was heard in keeping with a prosthetic aortic valve.
In early diastole an opening click was heard indicating that the mitral valve was a metal valve.
There was a pan-systolic murmur best heard at the mitral area and this radiated to the axilla confirming our earlier suspicion of mitral regurgitation.
On auscultation of the lung bases fine late inspiratory crepitations were heard in keeping with the earlier suspicion of left ventricular failure.
Diagnosis:
Prosthetic aortic and mitral valves
Mitral regurgitation
Atrial fibrillation, pulmonary hypertension, heart failure
Possibly infective endocarditis

Cardiovascular examination

2007-01-13T03:31:00.000-08:00

The patient was an elderly male. He was propped up in bed, looked breathless and had an oxygen mask on. At this point the trainee was asked what came to mind and she replied that in the context of being asked to examine the cardiovascular system, breathlessness suggested that the patient had heart failure or more precisely left ventricular failure.
He was of average height and weight.
There was no abnormality detected on examination of the head.
On examination of the hands the trainee noted tar staining of the fingers. We asked the trainee what her thoughts were and she replied that this would suggest that the lesion might be related to cigarette smoking (i.e.) ischaemic heart disease.
The pulse rate was 80 beats per minute, regular, normal volume, no variation in character; all pulses were equal and synchronous.
On examination of the neck the JVP was elevated 6 cms above the manubriosternal angle, no dominant wave. This was further evidence in favour of heart failure. The trachea was in the midline.
On examination of the chest, there were no deformities, no visible pulsations.
The apex beat was at the 6th left intercostal space in the anterior axillary line. It was thrusting in nature.
Several points were raised here. First was the importance of documenting that the trachea was in the midline. If this had not been done one could not have said that the heart was dilated, as one had not excluded displacement of the apex due to mediastinal shift.
The heart was dilated with a thrusting apex. This raised several possibilities.
Mitral regurgitation, aortic regurgitation or ventricular septal defect.
Ventricular septal defect was unlikely unless one considered an acquired defect due to myomalacia cordis.
Aortic regurgitation was not likely, as the pulse was not collapsing in nature. Hence the most likely lesion was mitral regurgitation.
There was no parasternal heave, no palpable heart sounds and no thrills
The first heart sound was soft making mitral regurgitation more likely. The second heart sound was normal. There were no added sounds.
There was a blowing pan systolic murmur at the mitral area, radiating to the axilla. This confirmed the diagnosis of mitral regurgitation.
On examination of the back, fine late inspiratory crepitations were heard at both lung bases confirming our initial suspicion of left ventricular failure.
Diagnosis:
Mitral regurgitation
Sinus rhythm
Left ventricular failure
One has to consider the aetiology of mitral regurgitation in this case.
It may be primary valvular disease or it may be secondary to ischaemic cardiomyopathy and stretching of the mitral valve ring (our initial suspicion on seeing the tar staining of his finger)
Learn the causes of mitral regurgitation

Neurology for MRCP PACES

2007-01-05T12:15:00.000-08:00

We saw an interesting neurology case yesterday
The patient was a middle-aged Asian male seated propped up in bed. He had an oxygen mask on but this was because he had a chest infection and this had no bearing on his neurological problem. He was obese.
We asked the trainees to examine the lower limbs.
On examination, the size of the lower limbs was definitely small in relation to the patients torso and upper limbs. The shape of the limbs was also of note. The upper part looked reasonably normal but there was progressive wasting from the proximal aspect to the distal aspect of the lower limbs. The trainees described this an inverted champagne glass appearance.
This brought up the possibility of a peripheral neuropathy.
Next, we examined the skin (integument). The trainees noted that there was loss of hair over the distal aspect of the lower limbs, the skin over the distal aspect looked shiny and erythematous, there was scaling of the skin and the nails were dystrophic.
At this point we asked the trainees to think about the diagnosis. They concluded that the trophic changes were most likely a consequence of peripheral neuropathy and in a middle aged obese Asian male the most likely cause was diabetic neuropathy. (The possibility of hereditary motor sensory neuropathy should also be borne in mind)
Examination of the motor system revealed wasting of the quadriceps and the distal
muscles. This was evidence in favour of a lower motor neurone lesion with the distal
aspect being more severely affected, hence most likely to be a peripheral neuropathy.
There were no involuntary movements.
There was no weakness of abduction or adduction of the hips but apart from this all
muscles were weak and ankle movements and movements of the big toe were
completely absent. Further evidence in favour of peripheral neuropathy.
The knee jerk was present although reduced but the ankle jerk was tendon reflexes
was absent even with reinforcement. More evidence in favour of
peripheral neuropathy.
As there was marked weakness of the lower limbs it was not possible to test
coordination.
Sensory examination revealed decreased sensation affecting all modalities with the
distal aspect of the lower limbs being affected maximally (stocking distribution).
Further evidence in favour of a motor sensory neuropathy.
Gait could not be examined, as the patient was unable to walk.
Diagnosis: peripheral neuropathy mixed motor and sensory likely cause diabetes
mellitus but with the other causes of mixed motor and sensory neuropathy also being
considered.

A breathless patient with a cardiovascular problem

2006-12-16T01:50:00.000-08:00

The medical students were asked to examine the cardiovascular system.
The patient was an elderly man who was propped up in bed and had an oxygen mask on. He was of average height but looked underweight.
The students were asked for their impression at this point and they remarked that the patient looked breathless. As they had been asked to examine the cardiovascular system it was likely the breathlessness was related to the cardiovascular system and hence they concluded that the patient probably had left ventricular failure.
On examination of the head they noticed flaring of the alae nasi, further evidence of respiratory distress and giving further weight to the idea that the patient had left ventricular failure.
On examination of his hands there was no gross abnormality. His pulse rate was 90 beats per minute, regular in rhythm good volume and normal character. There was no radio-radial or radio-femoral delay. This did not help us any further in our diagnosis.
When the students began to examine the neck they were asked what they would expect to find in this patient. They replied that his JVP (jugular venous pressure) was likely to be elevated. Indeed this was the case and the JVP was elevated 6 cms above the manubriosternal angle. There was no dominant wave. The trachea was in the midline the carotids were normal.
On examination of the chest, the apex beat was felt in the 5th left intercostal space at the midclavicular line. It was a diffuse impulse. This did not give any further clues to the diagnosis. There was no parasternal heave and no palpable heart sounds or thrills.
On auscultation, the first heart sound was soft. This indicated that the mitral valve was not competent. Hence the students quite correctly suspected mitral regurgitation.
The second sound was of normal intensity signifying that the aortic valve was probably normal and that there was no pulmonary hypertension.
There was a blowing pan systolic murmur best heard at the apex. More evidence in favour of mitral regurgitation. The murmur increased in expiration; mitral regurgitation. The murmur radiated to the axilla; mitral regurgitation.
There were no added sounds or extra-cardiac sounds
On examination of the back of the chest there were fine late inspiratory crepitations at both bases, more marked on the right hand side, confirming our initial suspicion that the patient had left ventricular failure. There was no sacral oedema
Diagnosis: Mitral regurgitation, left ventricular failure
We next went through the causes of mitral regurgitation and discussed how to work out the causes of mitral regurgitation by drawing a diagram of the mitral valve apparatus and working out what could go wrong with each component of it.

Cardiovascular Examination (MRCP PACES)

2006-12-10T02:36:00.000-08:00

The patient was a middle-aged lady seated up in bed. She had an oxygen mask on.
At this point we thought that as it was a cardiovascular examination the patient was likely to have left ventricular failure.
She was of average height and weight.
On examination of her head we noticed that she had a high arched palate.
There was no abnormality detected on examination of her hands. Her pulse rate was 55 beats per minute, regular in rhythm. It was low in volume and slow rising in character. At this point the diagnosis of aortic stenosis came to mind.
There was no brachio-radial delay.
On examination of the neck we noticed that her JVP was elevated 6 cms above the manubriosternal angle. This made us think that the initial impression that she had heart failure was correct.
On examination of her chest, the apex beat was at the 5th intercostal space just medial to the mid-clavicular line. There was no appreciable variation in character. No parasternal heave, no palpable heart sounds or thrills.
On auscultation the first heart sound was normal, the second heart sound was soft and single (further evidence in favour of aortic stenosis)
There was an ejection systolic murmur best heard at the aortic area and this murmur radiated to the neck (in keeping with aortic stenosis)
There were fine late inspiratory crepitations at both lung bases (in keeping with left ventricular failure)
Diagnosis: aortic stenosis with left ventricular failure

Chest Examination

2006-12-10T01:33:00.000-08:00

We asked the medical students to examine a patient.
The patient was seated next to his bed and had an oxygen mask on. The students concluded that this patient must be suffering from a condition that would cause respiratory distress.
He was of average height but looked thin. This made them think that it must be a chronic condition that could cause cachexia or a malignancy.
They also noticed that he had a productive cough and that the sputum pot on his bedside table was almost half full. This made them think that it was a chronic respiratory condition that caused a productive cough. They suggested chronic bronchitis or bronchiectasis. The patient did not look a “blue-bloater”. This left the possibility of bronchiectasis.
On examination of his head we noticed that his face looked very thin, his alae nasi were flaring (further evidence of respiratory distress) and he had pursed lip breathing (suggesting chronic distal obstruction).
On examination of his hands we noticed that his fingers were clubbed. This more or less made the diagnosis of bronchiectasis secure.
His fingers were also very severely tar stained. This made us think of the possibility of bronchial cancer as a consequence of prolonged cigarette smoking.
On examination of his neck we notice that it was thin and that the crico-sternal distance was reduced (further evidence of chronic obstructive pulmonary disease).
His chest looked hyperinflated and thin, there was a scar in the right subclavian region, which looked like a long line had been inserted (either as an emergency or for feeding, which was unlikely as he presumably had a working gut, or for chemotherapy, bringing up the possibility of bronchial cancer).
The respiratory rate was 26 per minute, the apex was difficult to palpate, respiratory movements were equal, vocal fremitus was equal on the two sides but reduced.
Percussion note was resonant, with reduced cardiac and liver dullness further evidence of chronic obstructive pulmonary disease.
Breath sounds were vesicular, reduced in intensity and there were coarse crepitations mainly at the right base (in keeping with bronchiectasis)
Diagnosis: bronchiectasis
We needed to think of bronchial cancer in view of our other findings.
The patient had been on chemotherapy but this was for oesophageal cancer, which was not resectable.

COPD

2006-12-02T01:10:00.000-08:00

The medical students examined a patient who had been admitted to the medical admissions unit.
On approaching the patient they noticed that the patient was dressed in hospital pyjamas. I asked them whether this was significant. We worked out that this would mean that the patient was admitted as an emergency and did not have time to pack a bag to bring in to hospital. Thus we concluded that this was an acute illness or acute exacerbation of a chronic illness.
The patient was seated up in bed with an oxygen mask on and did not appear perfectly comfortable. This was evidence of respiratory distress.
On examination of his head we noticed flaring of his alae nasi, further evidence of compromised respiratory function.
On examination of his hands there was no definite abnormality in particular no clubbing and no flapping tremor. His pulse rate was 100 per minute.
On examination of his neck we noticed that the trachea was in the midline but the cricosternal distance was reduced. The students correctly interpreted this as evidence of a hyper inflated chest and therefore airways obstruction.
We now knew that this patient had airways obstruction and respiratory distress as a consequence of this.
The students then proceeded to the foot end of the bed and looked at the patient’s chest. They noticed that it was barrel shaped; further evidence of obstructed airways and the fact that a change in shape had occurred would mean that this obstruction was chronic.
The diagnosis at this point was chronic obstructive airways (pulmonary) disease with and acute exacerbation.
We had noticed by this point that the patient had a productive cough and thus we inferred that the likely cause of the exacerbation of airways obstruction was an infection of the chest.
Vocal fremitus was reduced but equal
Respiratory movements by palpation were equal
Percussion note was hyper-resonant with decreased cardiac and liver dullness (further evidence in favour of airways obstruction)
Breath sounds were vesicular but reduced in intensity (indicating a degree of emphysema)
There were no added sounds
Diagnosis: acute exacerbation of chronic obstructive pulmonary disease probably caused by a chest infection

Respiratory Examination – Keeping it simple

2006-11-30T22:53:00.000-08:00

We examined a patient with a respiratory condition. I was teaching some final year students and the emphasis was on keeping it simple.
The patient was an elderly lady who was seated in bed. As the students helped to get her into position they noticed that her mobility was poor and they noticed that her hands were deformed. At this point we thought that she had poor mobility due to rheumatoid arthritis and that the likelihood was the respiratory condition was associated with rheumatoid arthritis (we accepted that is could be a totally unrelated condition).
Examination of the head was unremarkable.
On examination of the hands, the nails were normal the skin was hyperpigmented (we could not account for hyperpigmentation).
There was swelling and ulnar deviation of the metacarpophalangeal joints and there was z deformity of the right thumb. No redness, non-tender
The interossei were wasted and there was bilateral wasting of the thenar eminence.
At this point we thought that the patient had inactive rheumatoid arthritis of the hands with disuse atrophy and carpal tunnel syndrome (the patient confirmed that she did have carpal tunnel syndrome)
At this point we thought of the complications of rheumatoid arthritis affecting the lung and what came to mind were pulmonary fibrosis, pleural effusions and rheumatoid nodules (we discounted rheumatoid nodules as being unlikely)
On examination of the trachea we noted that the trachea was deviated to the right.
We discussed the causes of tracheal deviation; conditions pushing it to the right or pulling it to the left. Out of the two conditions that we had in mind in relation to rheumatoid arthritis we thought that could be fibrosis on the right pulling the trachea or an effusion on the left pushing the trachea (fibrosis was unlikely as this is usually bilateral)
On examination of the chest we noted no abnormality in size or shape but respiratory movement was decreased on the left side of the chest.
This made us think that the patient must have a left sided pleural effusion.
We completed examination of the lungs and noted decreased percussion note (dull) with decreased breath sounds and decreased vocal resonance at the left base.
Diagnosis: left sided pleural effusion due to rheumatoid disease
We had not accounted for the pigmentation of her skin but as she had rheumatoid arthritis we thought that one of the drugs she would be taking could be the culprit. She was on methotrexate. We looked up the formulary and sure enough one of the adverse effects of methotrexate was photosensitivity.

Importance of correct clinical method

2006-11-29T22:43:00.000-08:00

One of the medical students was asked to perform a neurological examination on a patient who had poor mobility.
His findings were of bilateral incoordination of movement with past pointing and dysdiadokokinesis. The diagnosis was a bilateral cerebellar lesion.
On approaching the patient we looked at his face and noticed that there was paucity of facial expression, a mask like facies. Immediately, the possibility of parkinsonism was raised.
Glabella tap was positive, again a sign in favour of parkinsonism.
We thought of examining the upper limbs.
There was no deformity or gross change in size of the limbs and the skin looked normal.
There was no wasting of muscles but the patient had a resting tremor of his hands.
Again a sign indicating parkinsonism.
The tone in his upper limbs was increased. It was rigidity of the cogwheel type. This more or less confirmed our diagnosis of parkinsonism.
Power was reasonable but there was bradykinesia and hence movement was impaired. Coordination was difficult to assess but appeared intact.
This was an important learning point; in neurological examination it is of utmost importance to follow the steps of the examination in order, as the detection of some abnormalities will interfere with further evaluation.

Clinical Method is Interesting and Enjoyable

2006-11-28T16:59:00.000-08:00

We had a very good teaching ward round with three final year students today. We went in to see an elderly gentleman who had been admitted with breathlessness and had been found to have abnormal liver function tests.
We began to examine the patient and when we looked at his tongue we saw multiple circinate ridges surrounding annular central areas of with loss of papillae. This was a condition the students had not seen before. It was a geographical tongue and did not need further investigation.
We looked at the neck and noticed that the jugular venous pressure was elevated to the angle of the jaw. The dominant wave was systolic and it was expansile laterally. We discussed the causes of this going into basic pathophysiology. An expansile systolic wave would indicate that both the pressure and volume in the right atrium increased during systole. This would mean that the tricuspid valve was not competent. Hence, at this point we had diagnosed that the patient had tricuspid regurgitation.
On palpation of the apex we noticed that the patient had a forceful thrusting apex beat. We discussed the causes of a thrusting apex beat and the next exercise was for one the students to palpate the radial pulse and answer whether the likely valvular lesion was aortic regurgitation or mitral regurgitation (ventricular septal defect was unlikely in view of the age, absence of a thrill, absence of cyanosis). As the patient did not have a large volume collapsing pulse the likely lesion was mitral regurgitation.
Immediately the student was asked to listen at the apex and confirm his diagnosis. He did hear a pan systolic murmur radiating to the axilla.
The next question was what the characteristics of the second heart sound would be. This was discussed and the students were able to work out that mitral valve disease would cause right heart failure if the patient had developed pulmonary hypertension in which case the second heart sound would be loud and single. We then discussed the pathophysiology of the loud second heart sound.
On further auscultation of the heart we also noted a third heart sound at the apex.
We then discussed the likely cause of the abnormal liver function tests and decided that it was most likely due to congestion of the liver as a result of right heart failure and tricuspid regurgitation. This is another important learning point; in a patient with hepatomegaly and abnormal liver function tests, always look for elevation of the jugular venous pressure!

Neurological Examination for MRCP PACES

2006-11-26T05:09:00.000-08:00

We went through examination of the upper limbs.
The main thing in neurology is to stick to the system. Go through every step without omitting anything and the diagnosis will come to you.
We went through the system in detail and after demonstrating the method one of the candidates went through the method with supervision.
It was very slow to start with but this is the case when learning a new method. With repeated practice one will speed up.
The patient had no abnormality of size and shape of the limbs and there was no abnormality of the skin. Thus we excluded a long-standing neurological deficit (i.e.) one that had developed in childhood (this would have interfered with growth of the limbs e.g. childhood poliomyelitis). A sensory deficit may have resulted in trophic changes in the skin. This is the reason why it is essential not to leave out these steps in the examination.
The position of the limbs at rest were normal, hence the patient was unlikely to have a motor deficit (e.g. stroke, nerve palsy). Again examples to stress the importance of this step.
There was no wasting of muscles (no lower motor neurone lesion)
No abnormal movements
Tone, power and reflexes were all normal
On examination of the right upper limb we noticed that the patient had abnormal coordination with past- pointing and dydiadokokinesis. No dysmetria.
No sensory deficit.
Diagnosis:
Right cerebellar lesion
We asked what the candidate would like to examine next and the answer was the eyes.
On examination of the eyes, nystagmus was noticed with the fast phase to the right.
The next question would be what are the likely causes of this patient’s right cerebellar lesion.
This is where preparation from books comes in. It is essential to learn the causes of cerebellar lesions, unilateral and bilateral. However, when preparing for exams it is essential to focus on the common causes in the region where one will be examined.
For example in the UK the focus should not be on post-malarial cerebellar syndrome!

Quick Diagnosis of Bronchiectasis

2006-11-25T01:09:00.000-08:00

We saw a middle-aged lady. She was propped up in bed and appeared breathless at rest. She was of average height but was quite thin.
At this point we began to think that she must have a chronic respiratory disease or disseminated malignancy.
On examination of her head the only abnormality was flaring of the alae nasi, which added to our impression that she was in respiratory distress. There was no cyanosis or polycythaemia.
Her fingers were clubbed .At this point we went through the causes of clubbing and sifted out the causes which could come on acutely such as lung abscess and empyema as we thought this was more likely to be a long standing condition.
We noticed by this time the patient had a productive cough and this made us think that bronchiectasis was one of the most likely diagnoses.
There was no abnormality detected on examination of her neck.
There was no abnormality of the size and shape of her chest; respiratory movements were equal on the two sides suggesting that it was not a localised lesion
Her respiratory rate was 26 per minute
Respiratory movements equal on palpation
Vocal fremitus equal on the two sides
Percussion note resonant and equal on the two sides, no decrease in cardiac or liver dullness
Breath sounds were vesicular there were coarse mid to late inspiratory and expiratory crepitations at both bases; confirming our initial suspicion that the patient had bronchiectasis.
Vocal resonance was equal on the two sides
On further discussion, the other candidate who had not examined the patient commented that he noticed the patient had a nebuliser by her bedside (indicating airways obstruction) and this together with the productive cough made him suspect that the patient had bronchiectasis.
The learning point here is to make use of all the information available.
Some clinicians say they have difficulty differentiating coarse from fine crepitations. Remember the timing of the crepitations is important in differentiating moist sounds originating in the bronchi from sounds originating in alveoli and in addition the moist bronchial sounds are usually altered if the patient is asked to cough.

Brachio-Radial Delay

2006-11-23T23:17:00.000-08:00

We saw an elderly gentleman and examined the cardiovascular system.
On examination of his head the only physical sign we noticed was that his palate was very high-arched.
There was no abnormality noted on examination of his hands.
His pulse rate was 70 beats per minute, regular in rhythm, low volume, slow rising.
This immediately made us think of aortic stenosis.
There was an appreciable delay between the brachial pulse and the radial pulse; brachio-radial delay. This physical sign too was in favour of aortic stenosis.
There was no abnormality noted on examination of his neck.
The praecordium looked normal. The apex beat was at the 5th intercostal space in the mid clavicular line and was of normal character.
The first heart sound was of normal intensity on auscultation but the second heart sound was soft. Another sign in favour of aortic stenosis.
There was an ejection systolic murmur, which radiated into his neck. This helped us confirm our suspicion that the patient had aortic stenosis.
The important learning points here are to recognise and correctly interpret the signs picked up early on in the examination of the cardiovascular system. The diagnosis was made on examination of the radial and brachial pulses and auscultation of the heart was used to confirm the diagnosis.

Upper Border of the Liver

2006-11-23T23:00:00.000-08:00

We saw an interesting physical sign during the teaching sessions.
The patient was an elderly man who was tall but very thin. His face was gaunt with sunken malar regions.
On examination of his hands we noticed that his fingers were clubbed, there was tar staining of his fingernails and he had bilateral Dupuytren’s contractures.
There were no physical signs of note when examining his neck. His chest appeared hyperinflated.
His abdomen was scaphoid in shape but the upper part was locally distended and this enabled us to note the lower edge of his liver about 3 fingerbreadths below the costal margin. This was confirmed by palpation.
The other point raised by the student who examined the patient was that the subcostal angle was splayed out and on the basis of this and the fact that his chest appeared hyperinflated he suggested that the patient had chronic obstructive pulmonary disease.
On percussion of the liver we noticed that the upper border was not at the 5th intercostal space in the mid-clavicular line but was much lower. Indeed, the percussion note was resonant right down to the costal margin.
The liver was not enlarged it was pushed down by the hyperinflated lungs!
This is an important learning point. Never say the liver is enlarged until you have percussed the upper border and made sure the liver is not displaced downwards.
The patient was thin due to alcoholism and self-neglect. He also had bronchiectasis and this was the cause of clubbing.

Preparation for MRCP PACES 1/2007

2006-11-21T22:50:00.000-08:00

The first patient we saw yesterday had a problem with his hands.
The first step was to through examination of the hands with emphasis on the locomotor system.
We stressed the importance of examining function, as the diagnosis was easily made on inspection alone.
The patient had easily identified rheumatoid deformity of the hands with ulnar deviation at the metacarpophalangeal joints. There was no evidence of active disease. He had quite marked loss of function and was unable to move his interphalangeal joints, metacarpophalangeal joints, make a fist or place his hands in the prayer position or reversed prayer position. Simple activities such as lifting a cup to his lips or unbuttoning his shirt were also impaired.
The diagnosis was inactive, deforming rheumatoid arthritis of the hands and wrists with marked functional impairment.
The second patient had a respiratory problem and we concentrated on getting examination technique right and teaching the system.
The patient was thin, had marked clubbing, pectum carinatum, decreased cardiac and liver dullness on percussion and coarse crepitations at the bases. He had a productive cough.
Diagnosis bronchiectasis
He told us that he had whooping cough as a child hence we were able to deduce the probable aetiology

Preparation for MRCP PACES 1/2007

2006-11-18T01:16:00.000-08:00

Yesterday we saw three cardiovascular cases.
One of the doctors who attended for teaching had come to the classes for the first time, so we went through the method of examination of the cardiovascular system with him.
Again the stress was on correct method and the importance of doing one thing at a time.
The first patient was an elderly man who was breathless at rest and obese. Breathlessness suggested heart failure.
He had flaring of his alae nasi again in favour of heart failure.
His pulse rate was 90 beats per minute regular, normal volume, no abnormality in character.
JVP was elevated to the angle of the jaw, no dominant wave. This too added evidence to the fact that he was in heart failure.
There was a midline sternotomy scar, made us think of valve surgery. The apex beat was not displaced.
The first heart sound was normal. There was a click instead of the native second heart sound and there was an opening click just after the first heart sound.
No murmurs.
On examination of the back he had sacral oedema. This was initially missed by the candidate but when he was shown how one should run one’s finger down the spine, actively think of any spinal deformity and then look for sacral oedema, it was easily picked up
The lung bases were dull to percussion but there were no crepitations.
Diagnosis:
Aortic valve replacement, probably due to degenerative disease and congestive cardiac failure
The second patient we saw was the lady with mitral stenosis discussed yesterday with the medical students (see below)
The third patient was a middle-aged lady, lying comfortably in bed. She was obese.
No abnormality of the head
Pulse 80 beats per minute, regular good volume.
Neck normal.
No abnormality on inspection of the praecordium. Apex not displaced, normal character.
The first heart sound was of normal intensity. The second heart sound too was of normal intensity. There were no added sounds.
There was a blowing late systolic murmur heard at the apex. This murmur radiated to the axilla bit was also heard well at the base of the heart.
Diagnosis:
Mitral valve prolapse
The normal intensity of the first heart sound suggests that the valve is closing normally and hence not incompetent. The murmur beginning late in systole suggests that there is prolapse of the mitral valve. There was no mid-systolic click, which would have added more evidence in favour of mitral valve prolapse.
The ECHO confirmed prolapse of the posterior leaflet of the mitral valve.

Clinical Skills Teaching for Medical Students

2006-11-16T22:37:00.000-08:00

I taught three final year students yesterday. We went through examination of the cardiovascular system.
As usual we began with instruction on the correct method of examination. I explained that there is no difference in the method used when teaching medical students and teaching doctors attempting higher examinations such as MRCP PACES. Examination of the cardiovascular system should be done using the same method whether one is a junior medical student or a very senior physician. The difference is the senior physician will do it much better. Just think, Michael Schumacher drives a car using the same method every driver uses, he just drives better!
We went through general examination, head, hands, neck and anterior aspect of the chest.
The patient had interesting physical signs.
Initially, the students mentioned that she had a heparin infusion running and on questioning they did come out with the assumption that this indicated that the patient had either a structural or function lesion of the heart, either a valvular abnormality or an arrhythmia.
The patient had a malar flush and the students were able to interpret that this indicated mitral valve disease, with pulmonary hypertension.
The patient was in sinus rhythm with a small volume pulse; hence at this stage we were able to work out that the mitral valve was probably stenosed.
There were no obvious physical signs in the neck.
The praecordium did not show any abnormality on inspection and the positive signs
were a loud first heart sound , an opening snap, a mid-diastolic murmur with
pre-systolic accentuation and a loud second heart sound.
These physical signs were difficult to elicit initially but after the students were asked to concentrate on each phase of the cardiac cycle they were able to correctly identify these physical signs. We did get the patient to do some exercise at the end and this did accentuate the murmurs.

Preparation for MRCP PACES 1/2007

2006-11-15T23:27:00.000-08:00

On Tuesday we examined a patient with a cardiovascular problem. As mentioned in the last post we concentrated on method. I asked the candidate to examine the patient and then commented on his technique and then demonstrated the correct method and then one of the other candidates went through the method and we watched and corrected at every step.
This may seem painstaking but this is very important, as wrong method is a sure way of failing the exam.
The case was very difficult, congenital heart disease with a single ventricle and multiple operations so I do not think discussion of the findings will be useful. Such cases, fortunately, are rare.
The main learning point was the importance of going through every step of the examination technique and noting the findings at each step instead of trying to do a lot at once.
When asked to examine the hands the candidate made no comment on any abnormality. But when asked to look at the size and shape of the hands everyone present, including two medical students, was able to pick up that the patient had arachnodactyly. Similarly, when asked to comment on the mouth, no abnormalities were seen. But, when asked to look at the hard palate in particular it was easily picked up that the patient had a high arched palate. Lastly, when the instruction was to run the fingers down the spine and note whether there was an abnormality, it was easy to pick up the fact that the patient had a kyphoscoliosis. In short, the patient had marfanoid features, which were easily missed unless one examined using the correct method.

Preparation for MRCP PACES 1/2007

2006-11-12T08:07:00.000-08:00

Last week we began teaching for the MRCP PACES February diet.
As this will be the first attempt for almost all of the candidates from our hospital we thought an early start would be essential.
As usual we started off with basic clinical skills.
I taught two candidates and took them to a patient with a condition involving abdominal examination.
We started off with a general examination and went through in detail how to perform a general examination.
As in the last post, I emphasised the importance of restricting the general examination to what can be performed by inspection from the end of the bed.
We next went through examination of the head, hands and neck.
I emphasised use of the system to examine the head and hands and we then went through how to quickly examine the relevant parts of the neck. Where palpation of the neck is concerned, I pointed out that either it should be done properly by asking the patient to sit up and palpate from behind or one should inform the examiners that one would defer examination of the neck to the end of the examination when one would ask the patient to sit up and one would then examine the neck from behind.
We went though how one would quickly inspect the chest and then proceed to perform a detailed examination of the abdomen. We went through every step of inspection, palpation, percussion and auscultation. No step was left out, as it is essential at this stage to ensure that technique is perfected.
Lastly, I said that the candidate should point out to the examiner that in practice on would routinely examine the inguinal region, the genitalia and perform a rectal examination. This should be done although it may seem redundant.
Next, we had a brief discussion regarding presentation. It is best to present one’s findings in the same order in which one examined the patient. This makes it less likely that one will forget positive findings and relevant negative findings.
We quickly discussed the diagnosis and the reasons for saying so and then had a quick discussion of the relevant investigations and treatment. We did not spend much time on these aspects the main emphasis was on clinical method and getting this right.
The patient was a young man who was quite thin and had pigmentation of his skin. He had a fine tremor of his fingers.
He had a nasogastric tube inserted through his nose. He was deeply icteric. He had cheilitis and angular stomatitis. He had white pseudomembranes on his buccal mucosa.
There was normal chest hair, no spider naevi and no gynaecomastia.
The upper abdomen was distended. He had normal distribution of body hair, no distended veins.
His liver and spleen were enlarged. There was no ascites, no bruits or venous hum.
There was no cervical, axillary or inguinal lymphadenopathy.
We went through the findings and what they meant.
He was emaciated and this could indicate chronic illness or lack of nutrition indicating alcoholism. Pigmentation could indicate malnutrition or chronic liver disease. Haemochromatosis was unlikely as the patient was too young.
The fine tremor also suggests alcoholism.
The nasogastric tube confirms our impression that he is malnourished.
Deep icterus makes us think of the causes of jaundice (haemolytic, hepatocellular, obstructive).
Cheilitis and angular stomatitis are further evidence of malnutrition.
The pseudomembranes suggest candidiasis. This raises the possibility of immunosuppression.
There are no features of chronic hepatocellular failure.
He has hepatosplenomegaly.
Now one has to analyse the cause.
Initially, we thought of alcohol abuse with consequent malnutrition. There were further features such as the tremor, which were in favour of this.
The candidiasis made us think of immunosuppression and blood borne viruses.
In a young patient with hepatosplenomegaly we should also think of the possibility of lymphoma.
In summary, the most likely diagnoses are:
Alcoholic liver disease (acute alcoholic hepatitis since he has features of acute hepatocellular failure)
Hep C , Hep B (with HIV) in view of immunosuppression
Lymphoma
The diagnosis was acute alcoholic hepatitis and the patient was on steroids and hence the cause of the candidiasis.
This led us to what should one revise in relation to this case.
Obviously, one should go through clinical method in relation to abdominal examination.
Next, one should revise all the causes of the various physical signs we elicited.
I emphasised that it would be unwise to go for the MRCP PACES exam without knowing all the causes of hepatosplenomegaly. Remember, however, out of the list of causes concentrate on the causes that are most likely in the centre at which you are taking the exam.

General Examination

2006-11-12T01:02:00.000-08:00

I was engaged in quite a bit of clinical teaching over the last couple of weeks and one thing that I noticed was that most students and doctors were confused about the exact nature of a general examination.
This was across a broad range of experience- second year students , final year students and senior house officers.
When asked to perform a general examination they would look for jaundice, anaemia, clubbing, cyanosis , oedema and lymphadenopathy.
When questioned from where they would perform the general examination , they would all say that this would be done from the end of the bed.
The next question would be how they would assess clubbing and lymphadenopathy from the end of the bed. This not possible. Even to say a patient has oedema one would need to demonstrate pitting and this cannot be done from the end of the bed.
General examination is the visual survey one performs from the end of the bed.
Do not attempt to examine a lot at this point.
Stick to assessing the patient's clothing and grooming, the posture of the patient, the state of growth , development and metabolism and look for any major changes in the integument.

History Taking

2006-11-11T01:06:00.000-08:00

History taking is the most important clinical skill. It is the starting point and without a good start one would be doomed to failure.
I asked one of the medical students who was in clinic with me what he understands by the word history in relation to patients.
His reply was excellent . A history is the story of the patients illness.
A good story is easy to understand and is interesting.
However, before telling the story one must obtain the story from the patient. The technique is called "History Taking". By using the word "taking" one accepts that this is an active process rather than a passive process of asking an open question and expecting the patient to tell the entire tale. If this was the case the technique would have been called "History Listening" !

Clinical Skills

2006-11-09T14:29:00.000-08:00

This blog will discuss clinical skills and how one may develop one's clinical skills