apologies for not seeing you at the end of the day today - got caught up in finals-related planning
as i remember we had to update on:
- causes of aortic regurgitation (in a memorable & useful way)
- how not to kill people with a sickle chest crisis
arun & amanda: can you add your responses as comments to this post please?
Salaam
PS can someone please forward a link to this site to louis - we had to investigate pulsus paradoxus
Monday, 14 June 2010
clubbing, weight loss in an elderly male smoker
anyone else want to add anything by commenting?
the main issues were:
- clubbing & its diagnostic utility
- the significance of clubbing & tar-staining in an elderly smoker
- the difference between MR & AS as systolic murmurs [how would you tell these apart?]
- the work-up of weight loss & diarrhoea
- the causes & consequences of loneliness
it is important to find out what happens to this chap
Salaam
the main issues were:
- clubbing & its diagnostic utility
- the significance of clubbing & tar-staining in an elderly smoker
- the difference between MR & AS as systolic murmurs [how would you tell these apart?]
- the work-up of weight loss & diarrhoea
- the causes & consequences of loneliness
it is important to find out what happens to this chap
Salaam
breathlessness in a 72 year old man
saaid presented a case of an elderly gentleman [did we get his ethnicity? - see previous post] with a short-ish history of breathless, and a significant history of past PEs
we reviewed the aetiology of SOB, dividing them into hyper-acute, acute and chronic causes
an systematic division (cardiac, respiratory, chest wall, neurological, haematological etc) was also noted
we noted that diagnosis of PE is best based on a formal scoring system, eg wells & geneva, and that clinical features of PE & alternative diagnoses are part of the score [there are data showing the appropriate use of scoring leads to fewer repeat events, eg roy et al 2006]
this gentleman had emboli confirmed on CTPA
we briefly discussed investigation, in particular examination, CXR & ECG findings. we did not look at D-dimers or VQ scans - he was severely hypoxic but not retaining C02
we briefly discussed LMWH, warfarin, thrombolysis & embolectomy as therapies
[as an aside this gentleman had a troponin of 0.2 - is this significant?]
i mentioned the algorithm in davidson's 21e as being useful
as lessons, we raised the following issues, amongst others:
- presenting patients/summarising patients
- ABGs
- causes SOB
- NYHA classes
- investigation PE
as action points, we endeavored to:
- list causes aortic regurg
- find out how not to kill patients presenting with a sickle chest crisis
- improve our skills in ABG interpretation by finding a good learning resource & looking at patients' results
- find out if there is a NICE guideline on PE (i don't think so - the is a BTS guideline)
- review Dr Dilworth's lecture on SOB
- read various bits of Kumar & Clark, Baliga [not only is he a professor in ohio, he also has an MBA!]
- review Medicine at a Glance
- see more patients with PE
- follow up our patient
we reviewed the aetiology of SOB, dividing them into hyper-acute, acute and chronic causes
an systematic division (cardiac, respiratory, chest wall, neurological, haematological etc) was also noted
we noted that diagnosis of PE is best based on a formal scoring system, eg wells & geneva, and that clinical features of PE & alternative diagnoses are part of the score [there are data showing the appropriate use of scoring leads to fewer repeat events, eg roy et al 2006]
this gentleman had emboli confirmed on CTPA
we briefly discussed investigation, in particular examination, CXR & ECG findings. we did not look at D-dimers or VQ scans - he was severely hypoxic but not retaining C02
we briefly discussed LMWH, warfarin, thrombolysis & embolectomy as therapies
[as an aside this gentleman had a troponin of 0.2 - is this significant?]
i mentioned the algorithm in davidson's 21e as being useful
as lessons, we raised the following issues, amongst others:
- presenting patients/summarising patients
- ABGs
- causes SOB
- NYHA classes
- investigation PE
as action points, we endeavored to:
- list causes aortic regurg
- find out how not to kill patients presenting with a sickle chest crisis
- improve our skills in ABG interpretation by finding a good learning resource & looking at patients' results
- find out if there is a NICE guideline on PE (i don't think so - the is a BTS guideline)
- review Dr Dilworth's lecture on SOB
- read various bits of Kumar & Clark, Baliga [not only is he a professor in ohio, he also has an MBA!]
- review Medicine at a Glance
- see more patients with PE
- follow up our patient
SNPing scientists
OK - i make no apologies for this post, even if it is not going to directly improve your performance in the end of year exams, this is such an important topic that i cannot let it go.
i find it laughable that you can graduate from 'London's Global University', the 4th best higher education institution in the world, with 3 science degrees (MB, BS, BSc), without knowing the significance of a SNP!
for those of you who might want to do science properly, this is crucial, for everyone else, this is part of the future of medicine
wikipedia has a simple explanation [be careful - the first google link takes you to the scottish national party]
Science hailed human genetic variation as the breakthrough of the year in 2007, and the lancet among others had the wellcome trust case control consortium genome-wide association scan as its paper of the year
[interestingly enough its breakthrough of the year 2009 was Ardipithecus ramidis, an early hominin species, that researchers published on last october (suwa et al, 2009) - they found a skeleton in 1994 & spent 16 years examining it - 'Ardi' a 50kg female lived 4-4.5 million years ago, about a million years before Australopithecus Lucy]
as william summerskill put it in an editorial:
"Despite the many excellent papers from prestigious scientific and medical journals, the choice this year was remarkably straightforward. After ranking the papers, more than half of The Lancet‘s editors had the same first choice: The Wellcome Trust Case Control Consortium’s Genome-wide association study of 14,000 cases of seven common diseases and 3,000 shared controls. Indeed, as soon as this study was published, the fi ndings created repercussions in the medical,6 scientific, and popular press."
the point about SNPs is that they represent a new way of working out human variation, one that was only possible because of the human genome project. more methods are coming, eg epigenetics. this is currently where we are at when it comes to 'personalised medicine', the holy grail of targeted, individualised diagnosis & therapy
when it comes to COPD, there has been some interesting work, for example looking at variants of an enzyme that breakdown extra-cellular matrix (MMP12), hunninghake et al 2009 (+ accompanying editorial by brusselle).
in this study a minor allele [do you know what this is?] was associated with some protection from developing COPD
there have been other studies looking at this & other genes on COPD & asthma (eg sleiman et al 2010, moffat et al 2007, he et al 2009)
a quick search on HapMap shows that the frequency of the AA genotype varies with population, for example 98% of the Japanese population have wild type AA (& therefore higher risk), while in the European population (actually taken from resident in Utah) it is only 80%
does this mean that Japanese people are at higher risk for COPD?
maybe - but MMP12 is only one part of the puzzle
whatever the answer in COPD, our 'stock' has a direct bearing on our health (& diseases) - and that is one reason to be aware of where we came from
Salaam
sabih
i find it laughable that you can graduate from 'London's Global University', the 4th best higher education institution in the world, with 3 science degrees (MB, BS, BSc), without knowing the significance of a SNP!
for those of you who might want to do science properly, this is crucial, for everyone else, this is part of the future of medicine
wikipedia has a simple explanation [be careful - the first google link takes you to the scottish national party]
Science hailed human genetic variation as the breakthrough of the year in 2007, and the lancet among others had the wellcome trust case control consortium genome-wide association scan as its paper of the year
[interestingly enough its breakthrough of the year 2009 was Ardipithecus ramidis, an early hominin species, that researchers published on last october (suwa et al, 2009) - they found a skeleton in 1994 & spent 16 years examining it - 'Ardi' a 50kg female lived 4-4.5 million years ago, about a million years before Australopithecus Lucy]
as william summerskill put it in an editorial:
"Despite the many excellent papers from prestigious scientific and medical journals, the choice this year was remarkably straightforward. After ranking the papers, more than half of The Lancet‘s editors had the same first choice: The Wellcome Trust Case Control Consortium’s Genome-wide association study of 14,000 cases of seven common diseases and 3,000 shared controls. Indeed, as soon as this study was published, the fi ndings created repercussions in the medical,6 scientific, and popular press."
the point about SNPs is that they represent a new way of working out human variation, one that was only possible because of the human genome project. more methods are coming, eg epigenetics. this is currently where we are at when it comes to 'personalised medicine', the holy grail of targeted, individualised diagnosis & therapy
when it comes to COPD, there has been some interesting work, for example looking at variants of an enzyme that breakdown extra-cellular matrix (MMP12), hunninghake et al 2009 (+ accompanying editorial by brusselle).
in this study a minor allele [do you know what this is?] was associated with some protection from developing COPD
there have been other studies looking at this & other genes on COPD & asthma (eg sleiman et al 2010, moffat et al 2007, he et al 2009)
a quick search on HapMap shows that the frequency of the AA genotype varies with population, for example 98% of the Japanese population have wild type AA (& therefore higher risk), while in the European population (actually taken from resident in Utah) it is only 80%
does this mean that Japanese people are at higher risk for COPD?
maybe - but MMP12 is only one part of the puzzle
whatever the answer in COPD, our 'stock' has a direct bearing on our health (& diseases) - and that is one reason to be aware of where we came from
Salaam
sabih
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