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
Saturday, April 21, 2007
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
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