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

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

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)

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)

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)

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

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

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.

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.

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

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.

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

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.

Importance of correct clinical method

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

Clinical Method is Interesting and Enjoyable

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

Neurological Examination for MRCP PACES

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

Quick Diagnosis of Bronchiectasis

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

Brachio-Radial Delay

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

Upper Border of the Liver

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

Preparation for MRCP PACES 1/2007

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