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.
Thursday, November 30, 2006
Wednesday, November 29, 2006
Importance of correct clinical method
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.
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.
Tuesday, November 28, 2006
Clinical Method is Interesting and Enjoyable
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!
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!
Sunday, November 26, 2006
Neurological Examination for MRCP PACES
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!
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!
Saturday, November 25, 2006
Quick Diagnosis of Bronchiectasis
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.
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.
Thursday, November 23, 2006
Brachio-Radial Delay
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.
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
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.
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.
Tuesday, November 21, 2006
Preparation for MRCP PACES 1/2007
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
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
Saturday, November 18, 2006
Preparation for MRCP PACES 1/2007
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.
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.
Thursday, November 16, 2006
Clinical Skills Teaching for Medical Students
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.
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.
Wednesday, November 15, 2006
Preparation for MRCP PACES 1/2007
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.
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.
Sunday, November 12, 2006
Preparation for MRCP PACES 1/2007
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.
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
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.
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.
Saturday, November 11, 2006
History Taking
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" !
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" !
Thursday, November 09, 2006
Clinical Skills
This blog will discuss clinical skills and how one may develop one's clinical skills
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