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
Saturday, June 23, 2007
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
Cardiovascular Examination for MRCP PACES
The patient was an elderly female lying propped up in bed. She was of average height and weight.
There were no abnormalities seen on examination of her head.
On examination of her hands there were no abnormalities found. Her pulse rate was 80 beats per minute, regular in rhythm and volume, normal character, all pulses were equal and synchronous.
On examination of her neck, the JVP was elevated to the angle of the jaw. The dominant wave was an expansile systolic wave. This made the trainee think of tricuspid regurgitation. The venous wave was under high pressure and palpable. This made the trainee think that the cause of the tricuspid regurgitation was right heart failure due to pulmonary hypertension. As the patient did not appear to have significant pulmonary disease the suspicion was that this was due to long standing left ventricular dysfunction.
The trachea was in the midline.
There were no abnormalities seen on inspection of the chest, the apex beat was palpable in the 6th left intercostal space lateral to the midclavicular line. This made the trainee think that either the patient had systolic heart failure or dilatation of the ventricle due to diastolic overload caused by valvular regurgitation. There was no thrust or heave at the apex and there was no parasternal heave.
The 1st heart sound was soft making the trainee think that the mitral valve was not competent. The second sound was also soft.
There was an opening snap heard best at the mitral area this made the trainee think that there was stenosis of the mitral valve.
There was an ejection systolic murmur radiating to the neck suggesting that the patient has aortic stenosis. There was a pan- systolic murmur at the left sternal edge and this increased with inspiration in keeping with tricuspid regurgitation. This had been suspected earlier on the basis of the characteristics of the JVP.
There was also a pan systolic murmur at the mitral area. This increased in expiration and radiated to the axilla in keeping with mitral regurgitation that had been suspected earlier on the basis of the soft 1st heart sound. There was a rumbling mid-diastolic murmur at the mitral area in keeping with mitral stenosis.
There was no sacral oedema and the lung bases were clear.
Diagnosis
Mitral stenosis
Mitral regurgitation
Aortic stenosis
Tricuspid regurgitation
Questions
How would you know whether the mitral stenosis or regurgitation was dominant?
In this case one would suspect that mitral regurgitation was dominant. The pulse was of normal volume, the apex beat was displaced and the first heart sound was soft (see table in ACES for PACES page 221)
How would you tell whether the aortic valve was severely narrowed?
The aortic stenosis was not severe in this patient because she had a normal volume pulse; there was no brachio-radial delay, no thrill, no fourth heart sound (see ACES for PACES page217)
Can a mid-diastolic murmur occur in mitral regurgitation?
Yes, severe mitral regurgitation can cause a flow murmur in mid-diastole (see causes of mid-diastolic murmurs ACES for PACES page211-212)
How do you know that this is not a flow murmur?
The patient has an opening snap, which would suggest stenosis of the mitral valve
Revision Tips
Revise auscultation of the heart ACES for PACES pages 204-222
Thursday, February 15, 2007
Neurology for MRCP PACES
The patient was a young man lying comfortably in bed
He was of average height and weight
On examination of the lower limbs the trainee noted that there was no major change in the overall size of the limbs and there were no trophic changes in the skin. These findings indicated that the lesion was not long standing.
The muscles of the lower limb were wasted; there were no involuntary movements. This suggested that the lesion affected the lower motor neurone. The absence of involuntary movement, in particular fasiculations, suggested that the anterior horn cell was not affected.
Tone was flaccid reinforcing the idea that this was a lower motor neurone lesion.
Power was decreased throughout the lower limb with the distal muscles being affected to a greater degree. In keeping with a lower motor neurone lesion. The distribution of the weakness was a paraparesis. What we had now demonstrated was a flaccid paraparesis. This narrowed the possibilities down to just a few (ACES for PACES page 452). Of these options, flaccidity narrowed the possibilities down even further leaving us with the possibility of either a radiculopathy or cauda equina lesion.
Reflexes were absent even with reinforcement, further evidence in favour of a lower motor neurone lesion. Eliciting reinforcement allowed us to see that the upper limbs were functioning normally reinforcing our idea that this was a paraparesis.
It was not possible to test coordination in the lower limbs in view of the weakness.
Sensory examination did not reveal a gross deficit; there was equivocal loss of light touch over the feet. This would be a feature against a cauda equina lesion, as the patient would have had anaesthesia in a saddle distribution.
The most likely diagnosis was a polyradiculoneuropathy.
The candidate was asked whether he would like to ask the patient a question regarding the condition to reinforce the diagnosis. The question was whether the patient’s bladder or bowels were affected. Although autonomic features are common in acute inflammatory demyelinating polyradiculoneuropathy (Guillain-Barre syndrome, AIDP) the bladder is not commonly affected whereas it is commonly affected in cauda equina lesions.
The candidate was also asked whether there was any other physical examination he would like to conduct to exclude a cauda equina lesion. The answer was per rectal examination and testing for anal tone, which would be reduced, and the anal reflex, which would be absent in cauda equina lesions.
Diagnosis
Flaccid paraparesis due to a polyradiculoneuropathy possibly acute inflammatory demyelinating (the onset was over a short duration) or Gullain- Barre syndrome
Revision Tips
Neurology is a difficult subject and is often considered daunting by most candidates attempting the PACES examination.
It is helpful to know the causes of the types of deficit that occur in neurological practice as this will enable one to localise the site of the lesion
Study the causes of wasting of muscles (ACES for PACES page 443)
Study the causes of flaccidity (ACES for PACES page 449)
Study the different types of distribution of muscle weakness (ACES for PACES page 451-453)
Study the patterns of sensory loss and their causes (ACES for PACES page 455-456)
He was of average height and weight
On examination of the lower limbs the trainee noted that there was no major change in the overall size of the limbs and there were no trophic changes in the skin. These findings indicated that the lesion was not long standing.
The muscles of the lower limb were wasted; there were no involuntary movements. This suggested that the lesion affected the lower motor neurone. The absence of involuntary movement, in particular fasiculations, suggested that the anterior horn cell was not affected.
Tone was flaccid reinforcing the idea that this was a lower motor neurone lesion.
Power was decreased throughout the lower limb with the distal muscles being affected to a greater degree. In keeping with a lower motor neurone lesion. The distribution of the weakness was a paraparesis. What we had now demonstrated was a flaccid paraparesis. This narrowed the possibilities down to just a few (ACES for PACES page 452). Of these options, flaccidity narrowed the possibilities down even further leaving us with the possibility of either a radiculopathy or cauda equina lesion.
Reflexes were absent even with reinforcement, further evidence in favour of a lower motor neurone lesion. Eliciting reinforcement allowed us to see that the upper limbs were functioning normally reinforcing our idea that this was a paraparesis.
It was not possible to test coordination in the lower limbs in view of the weakness.
Sensory examination did not reveal a gross deficit; there was equivocal loss of light touch over the feet. This would be a feature against a cauda equina lesion, as the patient would have had anaesthesia in a saddle distribution.
The most likely diagnosis was a polyradiculoneuropathy.
The candidate was asked whether he would like to ask the patient a question regarding the condition to reinforce the diagnosis. The question was whether the patient’s bladder or bowels were affected. Although autonomic features are common in acute inflammatory demyelinating polyradiculoneuropathy (Guillain-Barre syndrome, AIDP) the bladder is not commonly affected whereas it is commonly affected in cauda equina lesions.
The candidate was also asked whether there was any other physical examination he would like to conduct to exclude a cauda equina lesion. The answer was per rectal examination and testing for anal tone, which would be reduced, and the anal reflex, which would be absent in cauda equina lesions.
Diagnosis
Flaccid paraparesis due to a polyradiculoneuropathy possibly acute inflammatory demyelinating (the onset was over a short duration) or Gullain- Barre syndrome
Revision Tips
Neurology is a difficult subject and is often considered daunting by most candidates attempting the PACES examination.
It is helpful to know the causes of the types of deficit that occur in neurological practice as this will enable one to localise the site of the lesion
Study the causes of wasting of muscles (ACES for PACES page 443)
Study the causes of flaccidity (ACES for PACES page 449)
Study the different types of distribution of muscle weakness (ACES for PACES page 451-453)
Study the patterns of sensory loss and their causes (ACES for PACES page 455-456)
Saturday, February 03, 2007
Cardiovascular examination for MRCP PACES
The patient was a middle-aged man who was propped up in bed. He had an oxygen mask on. The fact that he appeared breathless made the trainees suspect that the patient may have left ventricular failure. He was of average height and weight.
On examination of his head he had flaring of his alae nasi, which gave the trainees further evidence of dyspnoea.
On examination of his hands there was clubbing which immediately brought up the suspicion of infective endocarditis.
His pulse rate was 90 beats per minute regular in rhythm. It was a large volume pulse and it was collapsing in nature. Sinus rhythm with a collapsing pulse made the trainee suspect that the patient had aortic regurgitation. Careful examination of the character of the brachial pulse revealed a Bisferiens pulse. This brought up the diagnosis of mixed aortic valve disease.
On examination of the neck the jugular venous pressure was elevated. the predominant wave was a systolic wave causing outward distension of the vein. The trainee though this was a V wave indicating tricuspid regurgitation. The trachea was in the midline.
On examination of the praecordium, the apex was palpable in the 6th intercostal space in the anterior axillary line. It was diffuse in nature. With the trachea in the midline the apex being palpable in the 6th intercostal space in the anterior axillary line indicated dilatation of the heart rather than mediastinal displacement. This would be in keeping with the suspicion of aortic regurgitation although it was not thrusting in nature.
On auscultation the first heart sound was soft suggesting mitral regurgitation.
The second heart sound was soft in keeping with aortic stenosis.
There was an ejection systolic murmur radiating to the neck and a blowing, decrescendo early diastolic murmur at the left sternal edge. Confirming our suspicion of mixed aortic valve disease. There was a blowing pan-systolic murmur at the mitral area that increased in intensity during expiration adding further evidence to the earlier suspicion that the patient had mitral valve disease (tricuspid regurgitation would have made the murmur increase in inspiration)
On auscultation of the ling bases there were fine late inspiratory crepitations in keeping with the earlier suspicion that the patient had left ventricular failure.
The trainee was then asked to listen over the femoral artery.
There was a systolic and diastolic bruit over the femoral artery, which confirmed the suspicion that the patient had aortic regurgitation.
Diagnosis
Mixed aortic valve disease (dominant regurgitation)
Mitral regurgitation
Tricuspid regurgitation
Possible infective endocarditis
Revision Tips
Revise character of the pulse (ACES for PACES page 194)
Revise differentiation of mixed valve disease (ACES for PACES pages 220-221)
Revise abnormalities of the femoral artery (ACES for PACES pages 223-224)
On examination of his head he had flaring of his alae nasi, which gave the trainees further evidence of dyspnoea.
On examination of his hands there was clubbing which immediately brought up the suspicion of infective endocarditis.
His pulse rate was 90 beats per minute regular in rhythm. It was a large volume pulse and it was collapsing in nature. Sinus rhythm with a collapsing pulse made the trainee suspect that the patient had aortic regurgitation. Careful examination of the character of the brachial pulse revealed a Bisferiens pulse. This brought up the diagnosis of mixed aortic valve disease.
On examination of the neck the jugular venous pressure was elevated. the predominant wave was a systolic wave causing outward distension of the vein. The trainee though this was a V wave indicating tricuspid regurgitation. The trachea was in the midline.
On examination of the praecordium, the apex was palpable in the 6th intercostal space in the anterior axillary line. It was diffuse in nature. With the trachea in the midline the apex being palpable in the 6th intercostal space in the anterior axillary line indicated dilatation of the heart rather than mediastinal displacement. This would be in keeping with the suspicion of aortic regurgitation although it was not thrusting in nature.
On auscultation the first heart sound was soft suggesting mitral regurgitation.
The second heart sound was soft in keeping with aortic stenosis.
There was an ejection systolic murmur radiating to the neck and a blowing, decrescendo early diastolic murmur at the left sternal edge. Confirming our suspicion of mixed aortic valve disease. There was a blowing pan-systolic murmur at the mitral area that increased in intensity during expiration adding further evidence to the earlier suspicion that the patient had mitral valve disease (tricuspid regurgitation would have made the murmur increase in inspiration)
On auscultation of the ling bases there were fine late inspiratory crepitations in keeping with the earlier suspicion that the patient had left ventricular failure.
The trainee was then asked to listen over the femoral artery.
There was a systolic and diastolic bruit over the femoral artery, which confirmed the suspicion that the patient had aortic regurgitation.
Diagnosis
Mixed aortic valve disease (dominant regurgitation)
Mitral regurgitation
Tricuspid regurgitation
Possible infective endocarditis
Revision Tips
Revise character of the pulse (ACES for PACES page 194)
Revise differentiation of mixed valve disease (ACES for PACES pages 220-221)
Revise abnormalities of the femoral artery (ACES for PACES pages 223-224)
Abdominal examination for MRCP PACES
The patient was a middle-aged man lying comfortably in bed. He was of average height. His weight was difficult to judge as his abdomen was distended but there appeared to be loss of weight as his extremities looked thin.
On examination of his head his sclerae were icteric making the trainee immediately suspect that the patient had liver disease. There were multiple telangiectasia over his face in keeping with hepatocellular failure. There was bilateral parotid enlargement which made the trainee suspect that the aetiology of the condition was alcohol abuse.
On examination of the hands there was palmar erythema another feature of hepatocellular failure. He had Dupuytren’s contracture, which was another feature that would suggest the aetiology of the condition was alcohol abuse.
He had multiple spider naevi over his upper chest a further indication of hepatocellular failure. There was no gynaecomastia and the distribution of hair growth over his chest was normal.
The abdomen was distended and the distension was greatest in the flanks this made the trainee suspect that the patient had ascites. There were visible veins on the anterior abdominal wall and the direction of blood flow was from caudal to cranial. This suggested that the patient had portal hypertension.
On palpation of the abdomen no lumps or organomegaly were detected. Percussion demonstrated a horseshoe shaped area of dullness and shifting dullness confirming the trainee’s earlier suspicion that the patient had ascites. Auscultation did not reveal any abnormality.
At this point the trainee was asked to employ the technique of “dipping” and with this technique she was able to note that the liver was enlarged three finger breadths below the costal margin but the enlargement was not detected by routine palpation because of the presence of ascites. This was an important learning point. In the presence of ascites always employ “dipping” to detect organomegaly or masses.
Diagnosis:
Features of chronic hepatocellular failure
Features of portal hypertension
Hence clinical diagnosis of cirrhosis of the liver
Aetiology probably alcohol abuse
Revision Tips
Learn the clinical features of cirrhosis of the liver (the features of hepatocellular failure, features of portal hypertension) the causes of cirrhosis of the liver and clinical clues to the causes of cirrhosis of the liver (ACES for PACES pages 305-306)
Learn the technique of “dipping” (ACES for PACES page 273)
On examination of his head his sclerae were icteric making the trainee immediately suspect that the patient had liver disease. There were multiple telangiectasia over his face in keeping with hepatocellular failure. There was bilateral parotid enlargement which made the trainee suspect that the aetiology of the condition was alcohol abuse.
On examination of the hands there was palmar erythema another feature of hepatocellular failure. He had Dupuytren’s contracture, which was another feature that would suggest the aetiology of the condition was alcohol abuse.
He had multiple spider naevi over his upper chest a further indication of hepatocellular failure. There was no gynaecomastia and the distribution of hair growth over his chest was normal.
The abdomen was distended and the distension was greatest in the flanks this made the trainee suspect that the patient had ascites. There were visible veins on the anterior abdominal wall and the direction of blood flow was from caudal to cranial. This suggested that the patient had portal hypertension.
On palpation of the abdomen no lumps or organomegaly were detected. Percussion demonstrated a horseshoe shaped area of dullness and shifting dullness confirming the trainee’s earlier suspicion that the patient had ascites. Auscultation did not reveal any abnormality.
At this point the trainee was asked to employ the technique of “dipping” and with this technique she was able to note that the liver was enlarged three finger breadths below the costal margin but the enlargement was not detected by routine palpation because of the presence of ascites. This was an important learning point. In the presence of ascites always employ “dipping” to detect organomegaly or masses.
Diagnosis:
Features of chronic hepatocellular failure
Features of portal hypertension
Hence clinical diagnosis of cirrhosis of the liver
Aetiology probably alcohol abuse
Revision Tips
Learn the clinical features of cirrhosis of the liver (the features of hepatocellular failure, features of portal hypertension) the causes of cirrhosis of the liver and clinical clues to the causes of cirrhosis of the liver (ACES for PACES pages 305-306)
Learn the technique of “dipping” (ACES for PACES page 273)
Friday, February 02, 2007
Cardiovascular case for MRCP PACES
The patient was an elderly female. She was lying propped up in bed and had an oxygen mask on. The trainees were asked what their impression was at that point.
Breathlessness in a patient with a cardiovascular problem was most likely to be due to left ventricular failure.
The patient was of average height but appeared to be thin. The trainee said that this probably indicated that the patient was cachectic on account of chronic illness.
On examination of the head the only physical sign of note was that the patient had flaring of the alae nasi in keeping with the suspicion of left ventricular failure.
On examination of the hands the trainee noted clubbing. In the context of the cardiovascular system there are few causes of clubbing. In the absence of cyanosis and in an elderly patient who was unlikely to have congenital heart disease (even after operative correction) the chances were the patient had infective endocarditis. There were no other peripheral stigmata of infective endocarditis.
The pulse rate was 80 beats per minute irregular in rhythm and volume indicating atrial fibrillation. Atrial fibrillation made the trainee suspect that the patient was likely to have mitral valve disease.
On examination of the neck it was noted that the jugular venous pressure was elevated and it was predominantly a systolic wave, which resulted in outward distension of the vein. This made the trainee think it was a V wave due to tricuspid regurgitation. A V wave in the context of atrial fibrillation and suspected mitral valve disease would raise the suspicion that the patient had right ventricular involvement secondary to the development of pulmonary hypertension as a consequence of mitral valve disease.
On examination of the praecordium it was noted that there was a midline sternotomy scar. This raised the possibility of valve replacement or bypass grafting.
The apex beat was displaced to the 6th intercostal space in the anterior axillary line. It was thrusting in nature. This would indicate that the left ventricle was dilated and there was diastolic overload. With the suspicion of mitral valve disease already raised on account of atrial fibrillation the most likely diagnosis at the moment was mitral regurgitation.
There was left parasternal heave and a palpable pulmonary second sound best felt at the pulmonary area. This was in keeping with the earlier suspicion that the patient had developed pulmonary hypertension as a consequence of mitral valve disease.
On auscultation of the heart the native first heart sound was replaced by a click indicating a prosthetic mitral valve.
The second heart sound was complicated. At the pulmonary area a loud native heart sound was heard in keeping with pulmonary hypertension. At the left sternal edge a click was heard in keeping with a prosthetic aortic valve.
In early diastole an opening click was heard indicating that the mitral valve was a metal valve.
There was a pan-systolic murmur best heard at the mitral area and this radiated to the axilla confirming our earlier suspicion of mitral regurgitation.
On auscultation of the lung bases fine late inspiratory crepitations were heard in keeping with the earlier suspicion of left ventricular failure.
Diagnosis:
Prosthetic aortic and mitral valves
Mitral regurgitation
Atrial fibrillation, pulmonary hypertension, heart failure
Possibly infective endocarditis
Breathlessness in a patient with a cardiovascular problem was most likely to be due to left ventricular failure.
The patient was of average height but appeared to be thin. The trainee said that this probably indicated that the patient was cachectic on account of chronic illness.
On examination of the head the only physical sign of note was that the patient had flaring of the alae nasi in keeping with the suspicion of left ventricular failure.
On examination of the hands the trainee noted clubbing. In the context of the cardiovascular system there are few causes of clubbing. In the absence of cyanosis and in an elderly patient who was unlikely to have congenital heart disease (even after operative correction) the chances were the patient had infective endocarditis. There were no other peripheral stigmata of infective endocarditis.
The pulse rate was 80 beats per minute irregular in rhythm and volume indicating atrial fibrillation. Atrial fibrillation made the trainee suspect that the patient was likely to have mitral valve disease.
On examination of the neck it was noted that the jugular venous pressure was elevated and it was predominantly a systolic wave, which resulted in outward distension of the vein. This made the trainee think it was a V wave due to tricuspid regurgitation. A V wave in the context of atrial fibrillation and suspected mitral valve disease would raise the suspicion that the patient had right ventricular involvement secondary to the development of pulmonary hypertension as a consequence of mitral valve disease.
On examination of the praecordium it was noted that there was a midline sternotomy scar. This raised the possibility of valve replacement or bypass grafting.
The apex beat was displaced to the 6th intercostal space in the anterior axillary line. It was thrusting in nature. This would indicate that the left ventricle was dilated and there was diastolic overload. With the suspicion of mitral valve disease already raised on account of atrial fibrillation the most likely diagnosis at the moment was mitral regurgitation.
There was left parasternal heave and a palpable pulmonary second sound best felt at the pulmonary area. This was in keeping with the earlier suspicion that the patient had developed pulmonary hypertension as a consequence of mitral valve disease.
On auscultation of the heart the native first heart sound was replaced by a click indicating a prosthetic mitral valve.
The second heart sound was complicated. At the pulmonary area a loud native heart sound was heard in keeping with pulmonary hypertension. At the left sternal edge a click was heard in keeping with a prosthetic aortic valve.
In early diastole an opening click was heard indicating that the mitral valve was a metal valve.
There was a pan-systolic murmur best heard at the mitral area and this radiated to the axilla confirming our earlier suspicion of mitral regurgitation.
On auscultation of the lung bases fine late inspiratory crepitations were heard in keeping with the earlier suspicion of left ventricular failure.
Diagnosis:
Prosthetic aortic and mitral valves
Mitral regurgitation
Atrial fibrillation, pulmonary hypertension, heart failure
Possibly infective endocarditis
Saturday, January 13, 2007
Cardiovascular examination
The patient was an elderly male. He was propped up in bed, looked breathless and had an oxygen mask on. At this point the trainee was asked what came to mind and she replied that in the context of being asked to examine the cardiovascular system, breathlessness suggested that the patient had heart failure or more precisely left ventricular failure.
He was of average height and weight.
There was no abnormality detected on examination of the head.
On examination of the hands the trainee noted tar staining of the fingers. We asked the trainee what her thoughts were and she replied that this would suggest that the lesion might be related to cigarette smoking (i.e.) ischaemic heart disease.
The pulse rate was 80 beats per minute, regular, normal volume, no variation in character; all pulses were equal and synchronous.
On examination of the neck the JVP was elevated 6 cms above the manubriosternal angle, no dominant wave. This was further evidence in favour of heart failure. The trachea was in the midline.
On examination of the chest, there were no deformities, no visible pulsations.
The apex beat was at the 6th left intercostal space in the anterior axillary line. It was thrusting in nature.
Several points were raised here. First was the importance of documenting that the trachea was in the midline. If this had not been done one could not have said that the heart was dilated, as one had not excluded displacement of the apex due to mediastinal shift.
The heart was dilated with a thrusting apex. This raised several possibilities.
Mitral regurgitation, aortic regurgitation or ventricular septal defect.
Ventricular septal defect was unlikely unless one considered an acquired defect due to myomalacia cordis.
Aortic regurgitation was not likely, as the pulse was not collapsing in nature. Hence the most likely lesion was mitral regurgitation.
There was no parasternal heave, no palpable heart sounds and no thrills
The first heart sound was soft making mitral regurgitation more likely. The second heart sound was normal. There were no added sounds.
There was a blowing pan systolic murmur at the mitral area, radiating to the axilla. This confirmed the diagnosis of mitral regurgitation.
On examination of the back, fine late inspiratory crepitations were heard at both lung bases confirming our initial suspicion of left ventricular failure.
Diagnosis:
Mitral regurgitation
Sinus rhythm
Left ventricular failure
One has to consider the aetiology of mitral regurgitation in this case.
It may be primary valvular disease or it may be secondary to ischaemic cardiomyopathy and stretching of the mitral valve ring (our initial suspicion on seeing the tar staining of his finger)
Learn the causes of mitral regurgitation
He was of average height and weight.
There was no abnormality detected on examination of the head.
On examination of the hands the trainee noted tar staining of the fingers. We asked the trainee what her thoughts were and she replied that this would suggest that the lesion might be related to cigarette smoking (i.e.) ischaemic heart disease.
The pulse rate was 80 beats per minute, regular, normal volume, no variation in character; all pulses were equal and synchronous.
On examination of the neck the JVP was elevated 6 cms above the manubriosternal angle, no dominant wave. This was further evidence in favour of heart failure. The trachea was in the midline.
On examination of the chest, there were no deformities, no visible pulsations.
The apex beat was at the 6th left intercostal space in the anterior axillary line. It was thrusting in nature.
Several points were raised here. First was the importance of documenting that the trachea was in the midline. If this had not been done one could not have said that the heart was dilated, as one had not excluded displacement of the apex due to mediastinal shift.
The heart was dilated with a thrusting apex. This raised several possibilities.
Mitral regurgitation, aortic regurgitation or ventricular septal defect.
Ventricular septal defect was unlikely unless one considered an acquired defect due to myomalacia cordis.
Aortic regurgitation was not likely, as the pulse was not collapsing in nature. Hence the most likely lesion was mitral regurgitation.
There was no parasternal heave, no palpable heart sounds and no thrills
The first heart sound was soft making mitral regurgitation more likely. The second heart sound was normal. There were no added sounds.
There was a blowing pan systolic murmur at the mitral area, radiating to the axilla. This confirmed the diagnosis of mitral regurgitation.
On examination of the back, fine late inspiratory crepitations were heard at both lung bases confirming our initial suspicion of left ventricular failure.
Diagnosis:
Mitral regurgitation
Sinus rhythm
Left ventricular failure
One has to consider the aetiology of mitral regurgitation in this case.
It may be primary valvular disease or it may be secondary to ischaemic cardiomyopathy and stretching of the mitral valve ring (our initial suspicion on seeing the tar staining of his finger)
Learn the causes of mitral regurgitation
Friday, January 05, 2007
Neurology for MRCP PACES
We saw an interesting neurology case yesterday
The patient was a middle-aged Asian male seated propped up in bed. He had an oxygen mask on but this was because he had a chest infection and this had no bearing on his neurological problem. He was obese.
We asked the trainees to examine the lower limbs.
On examination, the size of the lower limbs was definitely small in relation to the patients torso and upper limbs. The shape of the limbs was also of note. The upper part looked reasonably normal but there was progressive wasting from the proximal aspect to the distal aspect of the lower limbs. The trainees described this an inverted champagne glass appearance.
This brought up the possibility of a peripheral neuropathy.
Next, we examined the skin (integument). The trainees noted that there was loss of hair over the distal aspect of the lower limbs, the skin over the distal aspect looked shiny and erythematous, there was scaling of the skin and the nails were dystrophic.
At this point we asked the trainees to think about the diagnosis. They concluded that the trophic changes were most likely a consequence of peripheral neuropathy and in a middle aged obese Asian male the most likely cause was diabetic neuropathy. (The possibility of hereditary motor sensory neuropathy should also be borne in mind)
Examination of the motor system revealed wasting of the quadriceps and the distal
muscles. This was evidence in favour of a lower motor neurone lesion with the distal
aspect being more severely affected, hence most likely to be a peripheral neuropathy.
There were no involuntary movements.
There was no weakness of abduction or adduction of the hips but apart from this all
muscles were weak and ankle movements and movements of the big toe were
completely absent. Further evidence in favour of peripheral neuropathy.
The knee jerk was present although reduced but the ankle jerk was tendon reflexes
was absent even with reinforcement. More evidence in favour of
peripheral neuropathy.
As there was marked weakness of the lower limbs it was not possible to test
coordination.
Sensory examination revealed decreased sensation affecting all modalities with the
distal aspect of the lower limbs being affected maximally (stocking distribution).
Further evidence in favour of a motor sensory neuropathy.
Gait could not be examined, as the patient was unable to walk.
Diagnosis: peripheral neuropathy mixed motor and sensory likely cause diabetes
mellitus but with the other causes of mixed motor and sensory neuropathy also being
considered.
The patient was a middle-aged Asian male seated propped up in bed. He had an oxygen mask on but this was because he had a chest infection and this had no bearing on his neurological problem. He was obese.
We asked the trainees to examine the lower limbs.
On examination, the size of the lower limbs was definitely small in relation to the patients torso and upper limbs. The shape of the limbs was also of note. The upper part looked reasonably normal but there was progressive wasting from the proximal aspect to the distal aspect of the lower limbs. The trainees described this an inverted champagne glass appearance.
This brought up the possibility of a peripheral neuropathy.
Next, we examined the skin (integument). The trainees noted that there was loss of hair over the distal aspect of the lower limbs, the skin over the distal aspect looked shiny and erythematous, there was scaling of the skin and the nails were dystrophic.
At this point we asked the trainees to think about the diagnosis. They concluded that the trophic changes were most likely a consequence of peripheral neuropathy and in a middle aged obese Asian male the most likely cause was diabetic neuropathy. (The possibility of hereditary motor sensory neuropathy should also be borne in mind)
Examination of the motor system revealed wasting of the quadriceps and the distal
muscles. This was evidence in favour of a lower motor neurone lesion with the distal
aspect being more severely affected, hence most likely to be a peripheral neuropathy.
There were no involuntary movements.
There was no weakness of abduction or adduction of the hips but apart from this all
muscles were weak and ankle movements and movements of the big toe were
completely absent. Further evidence in favour of peripheral neuropathy.
The knee jerk was present although reduced but the ankle jerk was tendon reflexes
was absent even with reinforcement. More evidence in favour of
peripheral neuropathy.
As there was marked weakness of the lower limbs it was not possible to test
coordination.
Sensory examination revealed decreased sensation affecting all modalities with the
distal aspect of the lower limbs being affected maximally (stocking distribution).
Further evidence in favour of a motor sensory neuropathy.
Gait could not be examined, as the patient was unable to walk.
Diagnosis: peripheral neuropathy mixed motor and sensory likely cause diabetes
mellitus but with the other causes of mixed motor and sensory neuropathy also being
considered.
Saturday, December 16, 2006
A breathless patient with a cardiovascular problem
The medical students were asked to examine the cardiovascular system.
The patient was an elderly man who was propped up in bed and had an oxygen mask on. He was of average height but looked underweight.
The students were asked for their impression at this point and they remarked that the patient looked breathless. As they had been asked to examine the cardiovascular system it was likely the breathlessness was related to the cardiovascular system and hence they concluded that the patient probably had left ventricular failure.
On examination of the head they noticed flaring of the alae nasi, further evidence of respiratory distress and giving further weight to the idea that the patient had left ventricular failure.
On examination of his hands there was no gross abnormality. His pulse rate was 90 beats per minute, regular in rhythm good volume and normal character. There was no radio-radial or radio-femoral delay. This did not help us any further in our diagnosis.
When the students began to examine the neck they were asked what they would expect to find in this patient. They replied that his JVP (jugular venous pressure) was likely to be elevated. Indeed this was the case and the JVP was elevated 6 cms above the manubriosternal angle. There was no dominant wave. The trachea was in the midline the carotids were normal.
On examination of the chest, the apex beat was felt in the 5th left intercostal space at the midclavicular line. It was a diffuse impulse. This did not give any further clues to the diagnosis. There was no parasternal heave and no palpable heart sounds or thrills.
On auscultation, the first heart sound was soft. This indicated that the mitral valve was not competent. Hence the students quite correctly suspected mitral regurgitation.
The second sound was of normal intensity signifying that the aortic valve was probably normal and that there was no pulmonary hypertension.
There was a blowing pan systolic murmur best heard at the apex. More evidence in favour of mitral regurgitation. The murmur increased in expiration; mitral regurgitation. The murmur radiated to the axilla; mitral regurgitation.
There were no added sounds or extra-cardiac sounds
On examination of the back of the chest there were fine late inspiratory crepitations at both bases, more marked on the right hand side, confirming our initial suspicion that the patient had left ventricular failure. There was no sacral oedema
Diagnosis: Mitral regurgitation, left ventricular failure
We next went through the causes of mitral regurgitation and discussed how to work out the causes of mitral regurgitation by drawing a diagram of the mitral valve apparatus and working out what could go wrong with each component of it.
The patient was an elderly man who was propped up in bed and had an oxygen mask on. He was of average height but looked underweight.
The students were asked for their impression at this point and they remarked that the patient looked breathless. As they had been asked to examine the cardiovascular system it was likely the breathlessness was related to the cardiovascular system and hence they concluded that the patient probably had left ventricular failure.
On examination of the head they noticed flaring of the alae nasi, further evidence of respiratory distress and giving further weight to the idea that the patient had left ventricular failure.
On examination of his hands there was no gross abnormality. His pulse rate was 90 beats per minute, regular in rhythm good volume and normal character. There was no radio-radial or radio-femoral delay. This did not help us any further in our diagnosis.
When the students began to examine the neck they were asked what they would expect to find in this patient. They replied that his JVP (jugular venous pressure) was likely to be elevated. Indeed this was the case and the JVP was elevated 6 cms above the manubriosternal angle. There was no dominant wave. The trachea was in the midline the carotids were normal.
On examination of the chest, the apex beat was felt in the 5th left intercostal space at the midclavicular line. It was a diffuse impulse. This did not give any further clues to the diagnosis. There was no parasternal heave and no palpable heart sounds or thrills.
On auscultation, the first heart sound was soft. This indicated that the mitral valve was not competent. Hence the students quite correctly suspected mitral regurgitation.
The second sound was of normal intensity signifying that the aortic valve was probably normal and that there was no pulmonary hypertension.
There was a blowing pan systolic murmur best heard at the apex. More evidence in favour of mitral regurgitation. The murmur increased in expiration; mitral regurgitation. The murmur radiated to the axilla; mitral regurgitation.
There were no added sounds or extra-cardiac sounds
On examination of the back of the chest there were fine late inspiratory crepitations at both bases, more marked on the right hand side, confirming our initial suspicion that the patient had left ventricular failure. There was no sacral oedema
Diagnosis: Mitral regurgitation, left ventricular failure
We next went through the causes of mitral regurgitation and discussed how to work out the causes of mitral regurgitation by drawing a diagram of the mitral valve apparatus and working out what could go wrong with each component of it.
Sunday, December 10, 2006
Cardiovascular Examination (MRCP PACES)
The patient was a middle-aged lady seated up in bed. She had an oxygen mask on.
At this point we thought that as it was a cardiovascular examination the patient was likely to have left ventricular failure.
She was of average height and weight.
On examination of her head we noticed that she had a high arched palate.
There was no abnormality detected on examination of her hands. Her pulse rate was 55 beats per minute, regular in rhythm. It was low in volume and slow rising in character. At this point the diagnosis of aortic stenosis came to mind.
There was no brachio-radial delay.
On examination of the neck we noticed that her JVP was elevated 6 cms above the manubriosternal angle. This made us think that the initial impression that she had heart failure was correct.
On examination of her chest, the apex beat was at the 5th intercostal space just medial to the mid-clavicular line. There was no appreciable variation in character. No parasternal heave, no palpable heart sounds or thrills.
On auscultation the first heart sound was normal, the second heart sound was soft and single (further evidence in favour of aortic stenosis)
There was an ejection systolic murmur best heard at the aortic area and this murmur radiated to the neck (in keeping with aortic stenosis)
There were fine late inspiratory crepitations at both lung bases (in keeping with left ventricular failure)
Diagnosis: aortic stenosis with left ventricular failure
At this point we thought that as it was a cardiovascular examination the patient was likely to have left ventricular failure.
She was of average height and weight.
On examination of her head we noticed that she had a high arched palate.
There was no abnormality detected on examination of her hands. Her pulse rate was 55 beats per minute, regular in rhythm. It was low in volume and slow rising in character. At this point the diagnosis of aortic stenosis came to mind.
There was no brachio-radial delay.
On examination of the neck we noticed that her JVP was elevated 6 cms above the manubriosternal angle. This made us think that the initial impression that she had heart failure was correct.
On examination of her chest, the apex beat was at the 5th intercostal space just medial to the mid-clavicular line. There was no appreciable variation in character. No parasternal heave, no palpable heart sounds or thrills.
On auscultation the first heart sound was normal, the second heart sound was soft and single (further evidence in favour of aortic stenosis)
There was an ejection systolic murmur best heard at the aortic area and this murmur radiated to the neck (in keeping with aortic stenosis)
There were fine late inspiratory crepitations at both lung bases (in keeping with left ventricular failure)
Diagnosis: aortic stenosis with left ventricular failure
Chest Examination
We asked the medical students to examine a patient.
The patient was seated next to his bed and had an oxygen mask on. The students concluded that this patient must be suffering from a condition that would cause respiratory distress.
He was of average height but looked thin. This made them think that it must be a chronic condition that could cause cachexia or a malignancy.
They also noticed that he had a productive cough and that the sputum pot on his bedside table was almost half full. This made them think that it was a chronic respiratory condition that caused a productive cough. They suggested chronic bronchitis or bronchiectasis. The patient did not look a “blue-bloater”. This left the possibility of bronchiectasis.
On examination of his head we noticed that his face looked very thin, his alae nasi were flaring (further evidence of respiratory distress) and he had pursed lip breathing (suggesting chronic distal obstruction).
On examination of his hands we noticed that his fingers were clubbed. This more or less made the diagnosis of bronchiectasis secure.
His fingers were also very severely tar stained. This made us think of the possibility of bronchial cancer as a consequence of prolonged cigarette smoking.
On examination of his neck we notice that it was thin and that the crico-sternal distance was reduced (further evidence of chronic obstructive pulmonary disease).
His chest looked hyperinflated and thin, there was a scar in the right subclavian region, which looked like a long line had been inserted (either as an emergency or for feeding, which was unlikely as he presumably had a working gut, or for chemotherapy, bringing up the possibility of bronchial cancer).
The respiratory rate was 26 per minute, the apex was difficult to palpate, respiratory movements were equal, vocal fremitus was equal on the two sides but reduced.
Percussion note was resonant, with reduced cardiac and liver dullness further evidence of chronic obstructive pulmonary disease.
Breath sounds were vesicular, reduced in intensity and there were coarse crepitations mainly at the right base (in keeping with bronchiectasis)
Diagnosis: bronchiectasis
We needed to think of bronchial cancer in view of our other findings.
The patient had been on chemotherapy but this was for oesophageal cancer, which was not resectable.
The patient was seated next to his bed and had an oxygen mask on. The students concluded that this patient must be suffering from a condition that would cause respiratory distress.
He was of average height but looked thin. This made them think that it must be a chronic condition that could cause cachexia or a malignancy.
They also noticed that he had a productive cough and that the sputum pot on his bedside table was almost half full. This made them think that it was a chronic respiratory condition that caused a productive cough. They suggested chronic bronchitis or bronchiectasis. The patient did not look a “blue-bloater”. This left the possibility of bronchiectasis.
On examination of his head we noticed that his face looked very thin, his alae nasi were flaring (further evidence of respiratory distress) and he had pursed lip breathing (suggesting chronic distal obstruction).
On examination of his hands we noticed that his fingers were clubbed. This more or less made the diagnosis of bronchiectasis secure.
His fingers were also very severely tar stained. This made us think of the possibility of bronchial cancer as a consequence of prolonged cigarette smoking.
On examination of his neck we notice that it was thin and that the crico-sternal distance was reduced (further evidence of chronic obstructive pulmonary disease).
His chest looked hyperinflated and thin, there was a scar in the right subclavian region, which looked like a long line had been inserted (either as an emergency or for feeding, which was unlikely as he presumably had a working gut, or for chemotherapy, bringing up the possibility of bronchial cancer).
The respiratory rate was 26 per minute, the apex was difficult to palpate, respiratory movements were equal, vocal fremitus was equal on the two sides but reduced.
Percussion note was resonant, with reduced cardiac and liver dullness further evidence of chronic obstructive pulmonary disease.
Breath sounds were vesicular, reduced in intensity and there were coarse crepitations mainly at the right base (in keeping with bronchiectasis)
Diagnosis: bronchiectasis
We needed to think of bronchial cancer in view of our other findings.
The patient had been on chemotherapy but this was for oesophageal cancer, which was not resectable.
Saturday, December 02, 2006
COPD
The medical students examined a patient who had been admitted to the medical admissions unit.
On approaching the patient they noticed that the patient was dressed in hospital pyjamas. I asked them whether this was significant. We worked out that this would mean that the patient was admitted as an emergency and did not have time to pack a bag to bring in to hospital. Thus we concluded that this was an acute illness or acute exacerbation of a chronic illness.
The patient was seated up in bed with an oxygen mask on and did not appear perfectly comfortable. This was evidence of respiratory distress.
On examination of his head we noticed flaring of his alae nasi, further evidence of compromised respiratory function.
On examination of his hands there was no definite abnormality in particular no clubbing and no flapping tremor. His pulse rate was 100 per minute.
On examination of his neck we noticed that the trachea was in the midline but the cricosternal distance was reduced. The students correctly interpreted this as evidence of a hyper inflated chest and therefore airways obstruction.
We now knew that this patient had airways obstruction and respiratory distress as a consequence of this.
The students then proceeded to the foot end of the bed and looked at the patient’s chest. They noticed that it was barrel shaped; further evidence of obstructed airways and the fact that a change in shape had occurred would mean that this obstruction was chronic.
The diagnosis at this point was chronic obstructive airways (pulmonary) disease with and acute exacerbation.
We had noticed by this point that the patient had a productive cough and thus we inferred that the likely cause of the exacerbation of airways obstruction was an infection of the chest.
Vocal fremitus was reduced but equal
Respiratory movements by palpation were equal
Percussion note was hyper-resonant with decreased cardiac and liver dullness (further evidence in favour of airways obstruction)
Breath sounds were vesicular but reduced in intensity (indicating a degree of emphysema)
There were no added sounds
Diagnosis: acute exacerbation of chronic obstructive pulmonary disease probably caused by a chest infection
On approaching the patient they noticed that the patient was dressed in hospital pyjamas. I asked them whether this was significant. We worked out that this would mean that the patient was admitted as an emergency and did not have time to pack a bag to bring in to hospital. Thus we concluded that this was an acute illness or acute exacerbation of a chronic illness.
The patient was seated up in bed with an oxygen mask on and did not appear perfectly comfortable. This was evidence of respiratory distress.
On examination of his head we noticed flaring of his alae nasi, further evidence of compromised respiratory function.
On examination of his hands there was no definite abnormality in particular no clubbing and no flapping tremor. His pulse rate was 100 per minute.
On examination of his neck we noticed that the trachea was in the midline but the cricosternal distance was reduced. The students correctly interpreted this as evidence of a hyper inflated chest and therefore airways obstruction.
We now knew that this patient had airways obstruction and respiratory distress as a consequence of this.
The students then proceeded to the foot end of the bed and looked at the patient’s chest. They noticed that it was barrel shaped; further evidence of obstructed airways and the fact that a change in shape had occurred would mean that this obstruction was chronic.
The diagnosis at this point was chronic obstructive airways (pulmonary) disease with and acute exacerbation.
We had noticed by this point that the patient had a productive cough and thus we inferred that the likely cause of the exacerbation of airways obstruction was an infection of the chest.
Vocal fremitus was reduced but equal
Respiratory movements by palpation were equal
Percussion note was hyper-resonant with decreased cardiac and liver dullness (further evidence in favour of airways obstruction)
Breath sounds were vesicular but reduced in intensity (indicating a degree of emphysema)
There were no added sounds
Diagnosis: acute exacerbation of chronic obstructive pulmonary disease probably caused by a chest infection
Thursday, November 30, 2006
Respiratory Examination – Keeping it simple
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.
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.
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