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)
Friday, December 12, 2008
Friday, December 05, 2008
History Taking, Communication and Ethics for MRCP PACES
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
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
Sunday, November 23, 2008
Cardiovascular Examination
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
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
Monday, November 10, 2008
Respiratory Examination
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
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
Saturday, November 08, 2008
Cardiovascular examination
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
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
Sunday, October 14, 2007
Cardiovascular Examination for MRCP PACES
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.
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.
Sunday, September 30, 2007
Respiratory Case
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
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
Wednesday, August 08, 2007
Cardiovascular Examination for MRCP PACES
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)
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)
Saturday, August 04, 2007
MRCP (UK) Part 2 Clinical Examination (PACES) and Clinical Guidelines
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.
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.
Sunday, July 29, 2007
Presenting the Diagnosis in MRCP PACES
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
Sunday, July 22, 2007
MRCP PACES Respiratory Station
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.
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.
Sunday, July 15, 2007
Fail MRCP PACES physical examination stations
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
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
Saturday, June 23, 2007
Pass MRCP PACES
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
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
Saturday, June 02, 2007
History Taking, Communication and Ethics for MRCP PACES
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.
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.
Sunday, May 27, 2007
Cardiovascular Examination for MRCP PACES
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
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
Saturday, April 21, 2007
Cardiovascular Examination MRCP PACES
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
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
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)
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)
Saturday, April 14, 2007
Neurology for MRCP PACES
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
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
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
As usual teaching will concentrate on the basics, as this is what is needed to pass a clinical examination
Wednesday, February 21, 2007
Neurology for MRCP PACES
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
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
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