The old DundeeChest site spawned the AskDundeeChest website, back in the day. The students found it useful, I think. So I’ll set up another one on here.
Post a comment if you have a question, and I can answer the query on the main blog.
As Ron Pickering used to say……. “Away You Go”
I am just wondering if all of week 4’s lectures are going to be going up on dundee chest. Most of them are on blackboard but are these the up-to-date versions?
I have put up the most up to date versions of everything I have, on DC3.0. I have not received any slides from either of tomorrow’s lecturers – you will have to ask them why they haven’t provided the slides.
I will put up the exam chat from this morning, and some summary slides about TB, as that is what people asked about. But I’ll have to write them before I can put them up.
Is ARDS one of ILD?
the symptoms and signs for ARDS are quite similiar to acute interstitial diseases, but we (or just me?) keep thinking that ARDS and ILD as different disease.
My bad, found my answer. It is one of ILD.
Change of question:
why there is type II pneumocyte hyperplasia in acute ILD? (According to Underwood pathology book).
I thought is the reduce production of surfactants that causes pulmonary oedema…….etc
ARDS is not an interstitial lung disease, it is an end stage of acute lung injury, caused by a variety of pathological stimuli.
Acute Interstitial Pneumonia (AIP) is an interstitial lung disease that pathologically mimics ARDS very closely, but the two do not appear to be the same disease clinically.
I don’t know the answer to your second question – I suggest you ask Prof Carey.
I don’t understand your third comment, it doesn’t make sense.
Thanks.
It’s fine, I will ask Prof Carey about that. =)
Hello,
I just have a quick question regarding treatment for asthma. When you put a patient on regular inhaled corticosteroids do they also still take their Short acting Beta Agonist, when they require it or are they just kept on the regular Corticosteroid without the short acting beta agonist?
Patients always have some short acting beta agonist, as a reliever. The only exception is in those patients who receive Symbicort as maintenance and reliever therapy (SMART regimen).
There don’t seem to be any feedback forms on the blog or on BB. Are they anywhere particular, or do we just email the relevent staff?
Your options are:
Post your comments on the feedback page.
Send specific comments to Professor Lipworth
Send specific comments to me
Wait for the formal feedback forms to come around from the MSO.
Hello,
I have a question about lung cancer cell types (I hope it’s not too stupid). Small cell lung cancer has no chance of cure because it has a high mitotic rate and will therefore metastasise quite rapidly; whereas non-small cell lung cancer has a low mitotic rate and therefore, has a small chance of being treated depending on the staging of the disease. However, when we were doing haematology, when comparing Hodgkin’s lymphoma – which had a high mitotic rate – and non Hodgkin’s lymphoma – which had a low mitotic rate – there was a chance of curative treatment in high grade non-Hodgkin’s lymphoma, but not in low grade Non-Hodgkin’s lymphoma (i.e. it is the opposite of what happens in lung cancer). I just wanted to know why – is it that white blood cells behave differently compared to pneumocytes, or does it depend on clinical presentation, as you feel ill quite quickly if you have high grade non-Hodgkin’s lyphoma?
Thank you (and hope that my question makes sense)
Not a daft question at all. The key issue here is that chemothrapy for hodgkins is given with curative intent, but we have no chemo that cures SCLC.
Chemotherapy works by preventing cell division. In Lymphoma the more cells are dividing, the more chance there is of preventing cell division, so the more chance there is of curing the cancer. In SCLC the cells divide and grow rapidly, but our chemo doesn’t work as effectively, so the micro-metastases *will* develop into larger metastases with time, and lead, ultimately, to death.
I’ll ask an Oncologists to see if that’s anywhere near the right answer!
Hope you enjoyed the ward teaching today, and got something out of it!
Hi,
I don’t quite understand about TB.
As far as I know, primary TB is asymptomatic.
Does that means that all patient that were seen in hospital are secondary TB that due to reactivation? We can’t (or rarely) diagnose a primary TB?
And secondary TB occurs due to low immune competence. It can be weeks, months and even years (how can travel history helps in this case?).
For the patient that develops secondary TB after years, do they remains asymptomatic within the period? Do they usually in ‘end’ stage of disease because it usually spread to brain or miliary TB?
Or they can just recover without any complications?
Hi there,
I was wondering if you could tell me the difference between atelectasis and consolidation? Both seem to be caused by fluid collecting in the alveoli. Thanks!
Atelectasis is sub-segmental collapse of lung, due to either obstruction, poor ventilation, or fluid – http://en.wikipedia.org/wiki/Atelectasis
Consolidation is a bit of lung that has filled with fluid to become a solidified area – http://en.wikipedia.org/wiki/Consolidation_(medicine)
@DundeeChest: Thank you for the answer about cancer treatment and mitotic rates of a cancer type. I think I got mixed up between Hodgkin’s and high grade non-Hodgkin’s, but the answer still made sense. Also, yes, ward teaching was useful, thanks.
@Jun: From what I understand, primary TB is asymptomatic, or has mild symptoms – but not something that would make you suspect TB. They may get damage to the lung – but it’s usually small (Ghon focus). So you can’t really diagnose primary TB except in the rare cases where someone’s immune system is unable to deal with the TB antigen, and they get TB disease in the primary infection. If they have a positive tuberculin test and they haven’t had the BCG jab, I think you can say that they have been infected with TB at some point, but they don’t have the disease.
Secondary TB can be caused by either reactivation or reinfection. Reactivation is when the patient has latent TB and then at a time when they are immuno-compromised, or the immune system is weakened, the TB is reactivated and this causes the bacilli to multiply at a focus and you get TB disease (caseating necrosis etc). However, I think in a country like the UK, the chances of someone getting secondary TB due to reactivation is small (about 5-10%), but it’s more common in places where TB is quite commonly seen, so these people are asymptomatic, as they don’t have the disease. I think you get TB in the brain if there is a TB focus near the brain, but I’m not sure.
Secondary TB due to reinfection is when a person who has already been exposed to the disease gets another infection – so the bacilli are not latent – and despite previous exposure, the immune system is unable to contain the bacteria and you get TB disease. This is more common in the UK, so I’m guessing this is why we get told to ask about travel history.
Anyway, I hope that helps and that what I’ve written is right, If not, hopefully someone will correct it!
Thank you Yasmine! It does clear things up a bit!
But I’m not quite convince by ‘they have been infected with TB at some point, but they don’t have the disease’.
I read it somewhere that primary TB can progress to bronchietasis, effusion, pneumonia…etc. (or it that part of secondary TB?)
Is it because people with weak immune system, after first contact with TB, they progress into bronchietasis, effusion, pneumonia and even miliary TB?
Whereas people with normal immune system, remain asymtomatic. They healed and develop Ghon focus in the lung?
And the part for ‘caseating necrosis’, I THINK, even in primary TB, with or without progession, there still have caseating granulomas, where they will eventually heals, calcified and show up as Ghon focus in CXR.
Whereas in secondary TB, usually is cavitation in the lungs? (Can we see cavitation in CXR?)
Btw, can someone explain ghon focus and ghon complex? I know that ghon complex is the involment of both lung and nodal, means we can see that in primary TB? How about secondary TB? Is ghon complex a more serious clinical apperance that ghon focus?
*Sorry if all my questions sounds confusing!
Couldn’t put it in better way…
Latent TB – the Mycobacterium is resident in the patient, but does not cause infection. In the UK we do not treat latent TB. In the US they do. There is some recent evidence, from the US, that treating latent TB prevents subsequent infection.
Primary TB – the mycobacterium is resident in the patient, and causes infection. This can be in any organ, but is most commonly in the lungs. This primary infection can be fatal if left untreated. It can be fully, or partially cleared with treatment.
Secondary TB – either the mycobacterium is not fully cleared and reactivates, or there is a second infection in a cavity previously formed by primary TB.
TB should not infect normal lungs in an immunocompetent patient, so if a patient contracts TB it is likely they have either damaged lungs, or immuno-compromise of some sort.
Caseasting granulomas are the hallmark pathological finding of TB.
Lung cavitation can occur in primary or secondary TB, if left untreated.
Ghon focus – calcified granuloma.
Ghon complex – calcified granuloma and calcified lymph node.
Hi there,
I’ve been trying to figure out the difference between pulmonary oedema and consolidation. Am I right in thinking that pulmonary oedema is fluid in the alveolar space, but consolidation is just something in the alveolar space, that could be pus, fluid etc?
Does that mean pulmonary oedema is just a type of consolidation?
Thanks!
hey, attended the MDT last week and spoke to one of the oncologists and one of the chest surgeons, im trying to get in on one of the cancer resection losts, or single surgeries, whichever i can get. Ive got a request in to take a trip to edinburgh with some 4th years who are going to watch surgery. I was just wondering if there were any other oppertunities here in dundee you could point me towards, cheers
Euan
All the lung resection surgery is done in either Edinburgh, or Aberdeen.
Hi DC,
thanks for today’s talk illustrating the advantage of an SaO2 of 94-98% in increasing oximetry sensitivity to PaO2 changes. I’d also heard recently that maintaining oxygen saturation below 100% reduces free radical formation/damage and would like to know whether evidence for this exists and, if so, over what length of time it manifests itself?
Good question/comment. There is evidence that over oxygenation increases free radical production, along with evidence that renal blood flow, coronary artery blood flow, and cerebral perfusion are all reduced if there is excess oxygenation. The evidence is a mixed bag of animal models, and human studies, or varying quality and dubiety, but the volume suggests that it’s correct.
See BMJ last month for an argument about oxygen in ACS/MI. I’ll try to dig out the URL for the online version.
I’ve got a question about RoCE. For the CVS/RS/abdo examinations, should we be doing “full” examinations, examining what’s likely to show signs, just what’s on the clinical skills checklists, or a combination? Hope that makes sense,
Thanks,
A third year.
It depends on the case. It if is a respiratory case, I expect a full, thorough respiratory examination, but not necessarily a complete assessment of the neurological system. If the case is neurological, with no GI problems, an in depth neuro exam is more important than the GI exam.
What I want to see is evidence that you’ve thought about what information is important, and which is extraneous. What information helps to narrow the differential diagnosis, or strengthen the diagnosis.
Hi,
I was wondering if you could tell me HOW magnesium sulphate acts as a bronchodilator?
(I apologise if we have been taught this and I’ve just forgotten!)
I was wondering if the RoCE booklet could be typed or if it all had to be handwritten?
You can type it, just hand-write the clerking document part
*Transfering Medical school*
Hi there,
My husband has applied for medical jobs in Dundee – I am a Dundee 4th year, however if he doesn’t get a job in Dundee – how easy is it to transfer to A.N.Other Medical school closer to were he is appointed? Ideally I’d rather remain a Dundee medic (done 4 years now – and know the score), however understandably I’d prefer not to be seperated from my husband for weeks on end…. how easy is it to do Dundee 5th year placements in other UK hospitals (probably thinking south of the border) – and still qualify as a Dundee graduate?
I was wondering if you had any advice or comments on our situation.
Thanks,
MrsMedicalStudent
Please e-mail me with your actual e-mail address so I can arrange to meet up with you to discuss your options.
TCF
I tried to send this by email but I’m not sure if it has sent.
I am just putting everything together to finish my RoCE and we were sent the completion form on Friday by Susan Giel. There seem to be some discrepancies between what we have been asked to complete in the booklet and what we are asked to include on this Record of Completion sheet. For example, the sheet asks for an Infection control audit for outcome 5 but the booklet asks us to include a DPaC presentation for that outcome. Outcome 8 asks for feedback from a year 1 project but the booklet does not and outcome 9 seems to have taken a completely different format in the booklet to what is being asked for on the sheet. I just want to clarify on these things so I can include the right bits.
Hi Nathan
I’ve put answers on the RoCE blog, but in short.
The infection audit isn’t done any more, so don’t worry about it.
Outcome 8 – I suggest you put in the feedback.
Outcome 9 – do either of them
TCF
Hello,
Whilst writing up RoCE’s, a number of pneumonia patients presented classically with fluid in the lungs. I was wondering about the origin of such fluid. Was it initially vascular? Did cytokines initiate diapedesis that promoted extravasation of fluid – from the vessel to the sight of lung injury?
Many thanks,
Thomas
Hello,
I have heard a common question in the exam would ask what the ‘first line’ investigation is for something and what the diagnostic investigation is.
I was wondering if you could clear these terms up for me. Is first line just the first investigation you would do? (surely taking blood is frequently the first thing done)
and i suppose diagnostic is just the one that gives u a definitive diagnosis?
for example for TB would the first line be a chest x-ray? and the diagnostic test be a biopsy or sputum culture?
thanks
james
The first line investigation is the most useful test to do *first* – that test which helps to rule in your suspected diagnosis, or rule out as many others as possible.
The diagnostic test is the test which is most likely to give the diagnosis.
So in your case of possible TB, CXR is a good first line investigation, as a normal CXR essentially rules out TB. To make the diagnosis, you need sputum, or bronchial washings.
Hello, I was wondering if you could go over how to work out Aa gradients, maybe through an example?
Hi there
I was wondering where to find the radiotherapy tutorial that some of the older students made
Thanks
Jane
It’s a radiation tutorial, not a radiotherapy tutorial (You need Cancer Dundee for that).
If you search for radiation in the Search box on the right, it’s the second result down.
is diffuse pleural thickening pre-malignant to mesothelioma?
Thanks.
Hello, I too am having difficulty working out how to get an A-a gradient given an ABG and what amount of oxygen a patient is on (air – 15L). The lecture given by Dr. Stretton states A-a = PAO2 – (PaO2 + PaCO2/.08), he also gives a very rough guide equation to use A-a = InspO2 – (PaO2 + PaCO2). Going through the many examples later in the lecture, my calculations are never close to answers given in the “notes” section of the powerpoint. I think my issue is mainly finding out what PAO2 is. I am going to guess that PAO2 is not = to inspO2%? How do we calculate this out? Thanks.
Diffuse Pleural Thickening and Mesothelioma are separate entities. Pleural thickening my precede mesothelioma, but not necessarily.
The important thing to remember about A-a gradient is that you very rarely have to actually calculate it. A far more useful calculation is to work out what the pO2 should be: pO2 should be within 10 kPa of the FiO2, if gas transfer from the alveolus to the arteriole is perfect. This is because alveolar oxygen (PAO2) will be roughly 10 kPa lower than inspired oxygen (FiO2) because of the addition of water, and mixing with CO2.
So with an inspired O2 of air (21%), the pO2 should be greater than 11 kPa. If inspired O2 is 60 %, pO2 should be greater than 50 kPa. If the pO2 is less than it should be, it implies a defect in gas transfer.
You can use the full equation, if you want to, but in my clinical practice, I take 10 from the FiO2, and if pO2 is less than that number, there is a problem with oxygenation.
As usual, wikipedia is your friend
Hey, this has probably been mentioned before somewhere but I was wondering if we were expected to remember the normal values of o2, pH, anion gap etc or if they would be provided in the exam?
All normal values will be provided in all the exams, written and OSCE.
a quick pharm question i couldnt find the answer to, for prophylaxis of asthma, oral or inhaled steroid?
http://www.brit-thoracic.org.uk/Portals/0/Clinical%20Information/Asthma/Guidelines/qrg101%20revised%202009.pdf
Page 9
Hello,
I was just wondering is there any set first line investigation for diagnosing asthma? Or can it be either spirometry or PEFR?
Thank you.
http://www.brit-thoracic.org.uk/Portals/0/Clinical%20Information/Asthma/Guidelines/qrg101%20revised%202009.pdf
I was just wondering when we can expect to hear exam results from the medical school. Exams were last week so I’m not expecting to have heard yet, but was just wondering if there was a date when we could expect to hear by? Ta.
The Exam boards are on the 16th and 17th May, so you’ll not know until at least then.