Ask DundeeChest

There’s a new way to ask DundeeChest a question – rather than asking a question on this page, visit the new blog askdundeechest.wordpress.com.  By using a separate blog, I can keep some sort of order in the blog questions, and their answers.  It will also become searchable, and taggable, so it will be more useful.

So stop asking questions here, start asking questions here.

Here’s how to ask the DundeeChest team a question.  Whether you want a copy of the lecture you’ve just sat through, you don’t quite understand the difference between type 1 and type 2 respiratory failure, or you just want to chat to us, you can do it in a number of ways.

1.  Leave a comment on this page, and one of us will answer your query.

2.  Send an e-mail – click here to send an e-mail to us.  Make sure to put “Ask DundeeChest” in the title page

3.  Shout really loudly, preferably near East Block, and see if one of us answers

Thanks for playing!

72 Comments on “Ask DundeeChest”

  1. dundeechest Says:

    Hi DundeeChest,

    I didn’t quite understand what you were on about in the lecture this morning – cyanosis, anaemia, polycythaemia? Explain yourself!

    • dundeechest Says:

      OK – I’ll sort out a wee flash object to explain it all to you. Check back later in the week!

      DundeeChest

  2. Josh Scales Says:

    Dear Dr Fardon,

    I think I speak for most when I say we love your work, the enthusiasm and energy you have injected/aspirated into teaching.

    Thanks

    Josh

  3. Ross Says:

    In ITA our tutor said there was an assessment to do on-line before midnight on Friday, could someone enlighten as to the whereabouts of this assessment?

    Thanks!

    • dundeechest Says:

      The assessment is being uploaded to Blackboard today. It should be up there now, in fact.

      It’s a series of 10 multiple choice questions assessing the ITA work, and the lectures you’ve had during the week. This will be repeated throughout the block, with an assessment at the end of each week.

    • Dundee e-MedEd Says:

      Hi Ross – It will be uploaded tomorrow morning, we have to get the Learning Centre on main campus to upload it to Blackboard. Sorry for the delay. I will ask to see if we can extend the deadline given that’s it’s going up a bit late and post back here and post up an announcement in Blackboard too.

  4. Josh Says:

    Hi,
    I just got 45% which I was quite pleased with considering I didn’t feel there was much of what we covered in week one. 1 question on pharmacology and barely passable questions on physiology as they were testing fact recall, not understanding. Your thoughts?

    • dundeechest Says:

      Thanks for the comments.

      The first point I should make is that the questions were written by the lecturers for each specific lecture – they have chosen questions they feel best illustrate the important learning points from each topic.

      I vetted these questions and felt them to be fair, in that the knowledge and understanding required to answer the questions is appropriate to that of a second year medical student.

      The next point must be that the lectures are the starting point from which you can take forward your learning, just because the exact question was not covered in the lectures does not mean that there is no expectation that you should learn it. It is clear that part of the first week is to begin to understand what the clinical signs and symptoms are in respiratory medicine – you had only 2 lectures on this, but you have had private study time, and clinical sessions on the wards all week.

      I appreciate that you want to understand the topic, to work out the answers, rather than regurgitating facts – unfortunately, medicine requires both knowledge and understanding, and we test both.

      The formative assessment is meant to inform both us, the teachers, and you the students. You now know what we expect of you with respect to knowledge and understanding of respiratory medicine. We know now how much you have learnt, and whether we can provide further education tools to help you, and your peers.

      There is no pass mark for the assessment, there is no fail mark, the marks merely serve to show us, and you, how much information, and understanding you have assimilated over the past week.

      We have not provided a list of “Things you are expected to know and understand by the end of this week”, as we felt that as adult learners, you would make that decision for yourselves. If you, as a group, feel that you would like to have that information in a more didactic manner, let me know, and I can let you know what is expected of you.

      My advice prior to the next formative assessment, on COPD, Asthma, and Airways disease, mainly, is to read around the subject, follow the information provided in the blog, ask questions of your lecturers, ask questions on the blog, make the most of the iTA sessions by utilising the tutors, seek out help and advice, and be pro-active about your learning.

      I urge you, and your colleagues, to find the intended positives from this assessment tool – what did you learn, what did you understand, and when we asked something you weren’t expecting, why weren’t you expecting it?

      Finally – please keep commenting on the course, and the assessment tools. I really want this kind of feedback; we will not know how to approach this and other blocks in the future without knowing how you are finding it.

      Many thanks

      • Josh Scales Says:

        Thank you for your thorough reply it helpfully explains a lot. However you are covering your own backs by saying that combining work at school and at home one should have everything covered which is obvious and true. However, without trying to get caught up in the vitriol, we are adult learners but we are not respiratory consultants. Thus having covered 7 lectures on physiology and pharmacology respectively, it would be helpful to gauge how we are doing on the subjects, this seems pragmatic and reasonable. By the sounds of things this view is echoed by my peers, so will you take on board the views of students or will we have mutiny of the Dundee Chest Blog. As for the didacticism, listen to the people. I look forward to your reply and just to note I am still very much enjoying the course so thank you

        • dundeechest Says:

          Hi

          “Thus having covered 7 lectures on physiology and pharmacology respectively, it would be helpful to gauge how we are doing on the subjects, this seems pragmatic and reasonable. By the sounds of things this view is echoed by my peers, so will you take on board the views of students or will we have mutiny of the Dundee Chest Blog”

          I’m not sure I quite understand what the view is that you are trying to get across. Is it that you want to some way of gauging how you are doing in the subjects? That is why we’re doing the weekly assessments. In previous years you would have had to wait until the exam at the end of the year to find out if you know enough, now you (hopefully) get an idea after each week. You say you got 45% in the assessment, which suggest that you are half way there. Hopefully the people who got 10% went away, re-read the material, and had another crack at the assessment, and improved their score.

          If you feel there is a more practical way of letting you all know how you’re getting on through the week, please let me know. We could ask you all to write an essay on the putative benefits of prone ventilation, and a comparison of the mammalian and reptile respiratory apparatus, but that’s what I had to do 15 years ago, and I’m sure is not the best use of everyone’s time.

          We know that you’re not respiratory consultants, but we are not asking you respiratory consultant questions. The questions in the assessment were written to a phase 2 medical student standard, that is, what we would expect a second year medical student to know/understand.

          We’re not trying to cover our backs with anything – I am trying to provide you with the resources to learn. We are available for discussion, small group teaching, e-mail conversation, blog links, a chat over coffee or lunch all this month. Anyone can ask me anything about respiratory medicine, and probably about anything else too, and I will try to get the information to you as quickly as possible. But thus far, the blog comments have been about the unfairness of the test, or not being able to log on to blackboard etc. A poster earlier today (Annony Mouse, in fact) says that (s)he didn’t understand 1/10th of what the CCP session was about, but didn’t ask me to explain any of it, or arrange a tutorial, or ask for clarification, or a reference for where to go and read up on things. You can’t have it both ways (none of us can): if you want to learn, and you want to understand, we are ready to feed that hunger for this block; but if you don’t make use of the resources available to you, you don’t have the proverbial leg to stand on when the complaints start to be flung around. Perhaps no-one believes me that I’m here to teach – perhaps someone should just ask a question? What does Annony Mouse want to know?

          Didactism – you say listen to the people. People aren’t saying anything! You’ve not said your preference. Do *you* want me to stand up and give a lecture for 2 hours next Wednesday in the next CCP section? I can certainly do that if you want. My preference would be for a question and answer session on the core clinical problems, but it relies on the audience participating. I am listening; the line is currently static.

  5. Nadia Says:

    Hi
    I wasn’t able to access the respiratory formative over the weekend cause I couldn’t log in. I emailed access@dundee.ac.uk and got an email back this morning saying they’d sorted out the problem – but too late as formative has already been taken down. really wanted to have a go at it – could you email it to me?
    Thanks!

    • dundeechest Says:

      I understand that some people have had problems logging in. I also understand that these problems are now sorted. We will keep the session open until midnight tonight so you can complete the formative assessment at your leisure.

  6. Eilidh O'Neil Says:

    Hey
    As far as CCP goes I think today went fairly well but it would have been more useful at the end of the week when we’ve actually learnt about asthma/COPD. Having an interactive element was good but it would be helpful to have more lecture-y bits for when we clearly don’t get it. Definately NOT all online but if it could be posted up on blackboard afterwards please.
    Thanks for all your effort

    • dundeechest Says:

      The problem is, as I’m sure you’re fully aware, we have to teach it some sort of order. In an ideal world we’d do core clinical problem of chest pain after you’ve done PE, Pneumothorax, orthopaedics, psychiatry, gastroenterology, cardiology and surgery. But he have to do it now. The theory goes that if you do it with us now, when you come to do it with the cardiologists, you will know about PE and PTX, so they can talk about ACS, and the trick cyclists can talk about anxiety disorder.

      I know I keep banging on about this, but how are we supposed to know when it is that you “clearly don’t get it” if you don’t stick your hand up, or speak up and tell us that you don’t get it?

      What bit of today’s CCP didn’t you get? I’ll try to explain it on the blog, or I’ll sort out some extra sessions for you.

      Cheers

      Tom

      • Cardio/Resp Says:

        Firstly, when we “clearly don’t get it” refers to when the majority of the cohort selected the wrong answer during the CCP session on Monday – instead of being told WHY we were infact wrong all that was said was “yay” or “nay”… the majority of us not having a clue why this is the case! (and you are able to see how many of us “clearly don’t get it” – that is the very nature of having the interactive quiz is it not – you can see the answers that our cohort as a whole believe to be correct.)
        Secondly we have already covered CVS so therefore we already know what ACS is all about. Personally I prefered the way in which CVS was taught over Resp.
        Please can we have learning outcomes/objectives so that we know what it is that we are expected to know. In reference to your formative -there were actually 22 questions not the 10 you mentioned, is it possible that perhaps some of the questions were actually supposed to be asked at the end of week 2etc. but were mistakenly added to the week 1 formative instead?
        If you aren’t going to teach us all that we need to know, then please at the very least tell us HOW MUCH it is that you expected us to know/find out ourselves, ie how much detail is expected of us.
        Thanks.
        KM

        • dundeechest Says:

          OK. Thanks for commenting.

          I sat in on the second part of the CCP session so I could see how it went. The responses to the questions were actually pretty good, certainly no worse than the previous year’s cohorts. I totally agree that there should be more feedback and explanation of why you got it right or wrong, so I’ll try to correct that for Wednesday’s session.

          If you know all about ACS, and have it all sorted, then it should just be good revision. And that is half the point – each block should have CCP sessions in, and the CCPs should be revisited. Another commenter has said that the chest pain section was rushed, so you can see that I have to be able to accommodate the two extremes – you didn’t want to know about ACS, but another person in your group wanted to take more time over the chest pain section. Not easy.

          What was it about the CVS block you preferred? Perhaps we can adopt some of their practice?

          The block handbook has outcomes and objectives from each different bit, but we have never had to be so specific about outcomes and objectives for previous years, so I’m surprised by the requests for them this year. But that does not mean I can’t look into providing them. To be honest, the objectives will be basically be to learn and understand physiology, anatomy and pharmacology in the first week; and then learn and understand airflow obstruction, asthma, COPD, restrictive lung disease, acid base balance, and hyper-sensitivity.

          To be clear about the formative assessment – it is meant to inform all of you, and us, regarding your learning patterns, and how far we have to go. No-one should get worked up about not getting 100 % in the test, it should help your learning.

          I’m sure your last comment isn’t meant to sound as negative towards us as it reads at our end. My intention throughout the whole of this week and a half has been to make as much information available as possible to you all, either on line, face to face, extra sessions, answers in the blog etc, to add into the lectures and your own personal reading time. To say we are not going to teach you all you need to know is simply not true – everyone involved in the block is keen to provide as much as you ask for. As for how much detail – you’re all going to be doctors; you need to know it all, you need to know what a house officer knows, and you need to know it for your exams. The exams are at the end of the year – the formative assessment is in 3 days, you won’t get 100 %, but that’s not a problem, use the assessment to assist your learning.

          I’ll post on the main page the expectations we have for this week, to see if it helps.

          The assessment questions – there were only meant to be 10. I’ve looked at the feedback, and yes, you’re right, there were 22. That was the whole bank of questions that we asked main campus to pick 10 from. Great. Another cock-up. I’ll look into it further.

          Thanks for the comment.

  7. Jaz Says:

    Hi Dundee Chest,
    I was wondering if the CCP powerpoint could be made available on blackboard please?

    Thank you

    • dundeechest Says:

      Hi

      I have sent the Chest Pain one to the BlackBoard staff, and the Cough one should be up on there by tomorrow too.

      DC

  8. Josh Scales Says:

    Thank you again for an exemplary reply. Let me just explain that I think your approach is great and if my comments seem scathing its only because I am enjoy being able to openly discuss a subject that means a lot to me and one that I haven’t really been able to discuss before, that subject is our eduction. You are giving us a sense of autonomy which is fantastic. If I may make a generalisation about the classes, I think they want to be taught in a didactic manner, give them the information they need to pass (which I find frustrating). If it means anything I would talk to the group tomorrow repeating what you said above, if you want some help just pick on me, take the [—- ] and I will reply that kind of thing usually gets them going. Another way would get the group reps together and see whether they can precipitate your ideas and enthusiasm. Without going over the pharmacology and physiology content again I would ask the class what they thought. Cheers Josh

  9. Jaz Says:

    Hi DundeeChest,

    I was wondering if you could please explain the hypoxic drive to me? I understand that it is important in those with COPD, especially “blue bloaters” but I am confused about how it actually works!

    Thank you

    • dundeechest Says:

      OK. Hypoxic drive.

      There are three drives to respiration: stretch receptors; hypercarbia; and hypoxia.

      The first is stretch receptors – if the lungs do not move, the stretch receptors do not fire, and we have the sensation of being short of breath. Hold your breath, as if you were underwater – you can do that for about 40 seconds before you really can’t suppress the desire to breathe. If you have a sats probe on your finger while you hold your breath, the sats will not fall; likewise if you have a CO2 probe on, the level does not rise; so the drive to breath comes from not breathing (!). You can over-ride this with practice, so you can train yourself to swim further underwater.

      The second, and important in COPD and other forms of Chronic Type 2 respiratory failure, is hypercarbia. There are chemoceptors in the brain that respond to elevated levels of CO2, as the levels rise, there is increased stimulus to breathe. If I put you into a box, let you breathe through a circuit in which the CO2 is removed (Carbonate pellets), and slowly reduce your oxygen levels, you would not increase your respiratory rate for some time; but if I let your CO2 levels rise in the closed circuit, but top up the oxygen levels to keep them normal, your respiratory rate increases dramatically. People with type 2 respiratory failure have a chronically high CO2 – the chemoceptors reset their baseline, so high CO2 levels do not stimulate an increase in respiratory rate.

      This leaves the third drive to breathe, hypoxia. The theory goes like this: in a normal individual, during respiratory failure CO2 will rise and O2 will fall: the rise in CO2 leads to an increase in respiratory rate, which keeps brings up the O2 levels. In a patient with chronic type 2 failure, during an acute event, the patient will not increase their respiratory rate in response to an increasing CO2, so they rely on having low O2 levels to stimulate their breathing. If patients are therefore given too much oxygen, they are no longer hypoxaemic, and therefore have “lost their hypoxic drive”, and no stimulus to breathe, thus their CO2 rises when given too much oxygen So the theory goes. And that is the core knowledge, and I suppose is the learning objective for this bit.

      There is more to it than that, though. If you want to read more about a more detailed explanation for why patients with chronic type 2 respiratory failure retain CO2 when given too much oxygen, click the tag for V/Q Mismatch, or just click here.

      The concept of type 1, acute type 2, chronic type 2, and acute on chronic type 2 respiratory failure is not straightforward – I have SHOs and Registrars who still don’t quite get it. There will be a lecture on acid base balance on Friday, but if you want to get a head start on things, I’m giving a tutorial to the 4th years on Wednesday 23rd September at 1 PM in the East Block Seminar room on arterial blood gases, acid base balance, and respiratory failure. You’re welcome to join if you like.

  10. LDH Says:

    Just thought i should post about the CCP teaching block next week.

    I have to say I really enjoyed the first CCP on cough and felt that DR Nair (?) went through the processes associated with the diagnosis very well without getting too complicated. Hopefully I can use his way of reasoning his way the the diagnosis in future 🙂 I thought it was good of him to talk about why answers were incorrect rather than just saying what the answer was which has happened in the past.

    Could the next CCP be along the same line but perhaps with a wordsheet of conditions/word we must know….a glossary of sorts. Mabea it was my lack of knowledge but if I could know what I need to know before the lecture I could get a little bit more out of it.

    Many Thanks and I must say that I have enjoyed the rest of the block !!

    • dundeechest Says:

      Dear Lactate Dehydrogenase (arf)

      Thanks. I think we can certainly provide a handout, or something available for download suggesting the differentials of each core clinical problem, no worries.

      The CCPs for Wednesday next will be breathlessness, haemoptysis and headache, if you want to get a head start on the reading!

  11. ashinyapple Says:

    ‘DundeeChest’,

    A bit of light entertainment.

    Challenge extended:

    Patient presents with –

    An eastern european jewish infant develops mental retardation, loss of previously acquired motor skills, feeding difficulties, low tone in muscles, poor head control, and megalocephaly.

    Discuss and diagnose.

    Ashinyapple + the rest of the orchard

    • dundeechest Says:

      Rosh, my little Cox’s Pippin. You know how much of a paediatrician I am.

      But.

      If it weren’t for the megalencaphaly, the first thing to do is rule out menigo-encephalitis, and a space occupying lesion. Given it’s a small infant, you should probably think about intra-cranial haemorrhage too. A CT or MRI brain should help with the SOL, and haemorrhage (And hydrocephalus for the megalenchaphalus differential too), and given that it’ll need a GA for either, you could do the LP at the same time.

      But given the megalencephalus, you’d have to think about Megalencaphalic Leukodystrophy, particularly given the heavy handed hint about him being jewish, but it’s most common in Israelis, I believe. I’m not really sure about the incidence in Eastern Europeans, but the symptoms you describe fit.

      Differential of macrocephaly, off the top of my head
      Congenital – various unusual things, like MLC
      Hydrocephalus – either communicating or non-communicating
      Klinefelter’s syndrome
      Alexander Syndrome
      Idiopathic (of course)

      That’s my microcephalic nut emptied of paediatric knowledge for now.

      Anything above the diaphragm, below the larynx, in adults? Thanks for playing!

      • ashinyapple Says:

        Who or what is this ‘Rosh’ you speak of?

        Unfortuantely you didn’t win the large teddy this time! Perhaps next time.

        ShinyApple

        • Xander5 Says:

          Although not a particularly pleasant diagnosis is it Krabbe’s Disease? Possibly not but just a thought…

  12. laura Says:

    Hi Dundee Chest,

    Not sure where to post this question, but reading above – it appears this page is home to good mix of things and is really a general ‘ask anything’ kind of section!

    So…in the Respiratory System Phase Guide there are weekly clinical problems / patient cases with questions.
    Now, i appreciate we are ‘adult learners’ and all however, we are also creatures of habit and i know i sometimes get a little confused as to what’s expected! Last block, these ‘cases of the week’ were exactly that – a room booked for groups to discuss the case at the start of the week, and then a tutor facilitated session at the end of the week to discuss answers. I know my group got into the habit of meeting together initially, sharing out questions then coming together again and learning from one another. I certainly found learning this way really beneficial – and often found myself going beyond what was expected as ‘core’ knowledge.
    I’m sure I speak for others when I say we’re grateful for all the extra study time this block but could i clarify what is expected of us r.e. these case and whether answers will be provided?

    Thank you!

    Laura

  13. appleopolis Says:

    A general observation to some of the above….
    A wise and scary neurologist once told our year group:
    ‘knowing that you know something is of little value’
    ‘not knowing that you don’t know something is dangerous’ but
    ‘knowing that you don’t know something is of the most value’

    At the time this was perhaps the most frustrating and useless comment i had ever been told – but now it’s obvious how important a concept it is.
    So is 10% in a formative test better than 90%? You might not think so if the football is about to start, but if that means you do a little extra reading into a subject ‘we never got taught’ come your true clinical years – or your exams it might just help you ooot.
    x

  14. mOz Says:

    Just a quick question about todays Overview of Pulmonary Investigations lecture.

    Why do people with Restrictive LD have a normal PEFR ?? I would have thought that it would, as in Obstructive LD lead to a decrease.

    I understand that they will have a normal FEV1/FVC ratio.

    • dundeechest Says:

      Peak Expiratory Flow is a measure of large airway calibre: flow is related to radius of any tube to the 4th power, so the best flow is from the proximal airways, as they are largest. Peak flow happens very early in expiration as this flow comes from the larger airways. In early fibrosis the interstitium contracts and pulls the large airways to make them even larger, thus in early fibrosis the PEF actually gets larger! The lungs get smaller with worsening fibrosis, but the airways remain large, so flow rates remain normal (ish).

      FEV1 is a not a measure of flow, but of volume expired in forced expiration; the proportion of FEV1 to FVC is maintained in restrictive disease, but as the lungs shrink, the FEV1 falls too.

  15. daz Says:

    Hi I was wondering if we could arrange a session to discuss the clinical problems of the week that I have found in the booklets. I have had a bash but I would like to know if my brain is anywhere near the truth…

    Many thanks for all your efforts…you take quite a bashing on the board i notice (not justified in my opinion)!

    • dundeechest Says:

      Hi Dazzler

      I’m sure we can sort out a session. Tuesday afternoon, the earlier the better, or Wednesday between 1 and 3. Let me know when, and I’ll book a room.

  16. Asimo Says:

    helooooooooo!!
    I’m having trouble working out Slide 12/16 of the ‘Pulmonary Functions Test’ lecture By Dr. Lipworth.
    I’ll just copy n past the slide below to make things easier..

    ——————————————————
    STATIC LUNG VOLUMES

    Effort independent test
    Helium dilution / N2 washout : functional residual capacity
    (RV = FRC – ERV) (TLC = VC + RV)
    TLC in hyperinflation (Emphysema)
    TLC in restrictive lung disease
    Gas trapping in COPD:
    (RV/TLC%) (RVC – FVC/RVC%)
    TLC adds little to RVC and FVC
    ——————————————————

    I just don’t understand what some of the terms stand for… help!

    Cheers in advance!

    • Asimo Says:

      kk so i’ve posted the same thing twice.. i cant work these forum things… please delete one?:P cheers!

    • dundeechest Says:

      STATIC LUNG VOLUMES
      Here’s some translation:
      Effort independent test This means the tests are not dependent on effort. I’m not trying to be clever, it’s just to point out that theses tests should not be so dependent on how hard the patient tries. They still require the patient to be able co-ordinate the manouevre
      Helium dilution / N2 washout : functional residual capacity Two different methods of measuring lung volumes are via Helium Dilution, and Nitrogen Washout. The exact methods are not really core knowledge, but you can read up on them if you want
      (RV = FRC – ERV) (TLC = VC + RV) Residual Volume = Functional Residual Capacity – Expiratory Reserve Volume, Total Lung Capacity = Vital Capacity + Residual Volume
      TLC in hyperinflation (Emphysema) Total Lung Capacity goes up in emphysema because as the lung tissue is destroyed, the volume of air left inside gets bigger
      TLC in restrictive lung disease Total Lung Capacity goes down in restrictive lung disease because as the lung shrinks with the fibrosis, the lung volume falls
      Gas trapping in COPD: Gas trapping is due to areas of lung not being ventilated properly. Instead of having many small alveoli, there are fewer, bigger ‘ravioli’ – to enable adequate ventilation, the patient must breathe higher up their IRV as this keeps the alveolar walls under increased stretch. As this occurs, the Residual Volume increases in greater proportion to the TLC, therefore the TV/TLC ratio goes up.
      (RV/TLC%) (RVC – FVC/RVC%) I’m not sure why he’s talking about relaxed vital capacity minus force vital capacity over relaxed vital capacity, it’s not a measure I use clinically
      TLC adds little to RVC and FVC I’m not sure that I agree entirely with this statement. In patients with COPD in which they have mainly emphysema, the spirometry can be normal, but the TLC, and particularly, the RV/TLC ratio are increased. This is the so-called ‘normal spirometry COPD’ which is more common that you’d think!

      Does this help, or would you like me to ask BJL to clarify things?

      DC

  17. Sarah Macpherson Says:

    Hi – i didnt understand a couple of the points from the lecture this morning, was hoping someone could help.
    In severe COPD, the relaxed vital capacity is greater than the forced vital capacity. Why is this?

    From the pulmonary function lecture this morning, I didnt understand slide 6 about flow volume curve patterns. Why is there a different curve pattern for asthma (volume dependent airway closure?) and copd (pressure dependent airway closure?)

    Thanks
    Sarah

    • dundeechest Says:

      Hi Sarah,

      First question is pretty straightforward. In COPD the medium sized airways are collapsible – during forced expiration the medium sized airways collapse and leave air trapped behind the collapse; but during a relaxed manoeuvre the medium sized airways do not collapse, so theoretically the lungs should empty, thus Relaxed VC is greater than Forced VC in COPD.

      The second question is more difficult to answer. And given that my tea is ready, I’ll get back to you!

      DC

  18. Rachel Says:

    Hi,

    I am slightly confused by slide 6 of Dr Murphy’s Acid-base lecture. There are 4 equations and I understand that the first one is the carbonic acid:bicarbonate buffer system but what are the other 3 for? Are they equations for different buffer systems in the body? Which ones?

    H+ + HCO3- H2CO3 CO2 + H2O
    H+ + Hb- HHb
    H+ + HPO42- H2PO4-
    H+ + NH3 NH4+

    Thanks,

    Rachel

    • Rachel Says:

      oh sorry the arrows apparently don’t work on this but hopefully its not too hard to figure out!

    • dundeechest Says:

      Hi Rachel,

      There are 4 main buffer systems in the body. Haemoglobin is the main one – it is a large protein with many negatively charged parts, so is able to buffer a large number of H+ ions. Essentially, Hb keeps pH around 7.5. Hb doesn’t change very much, and certainly doesn’t change in response to acid base balance, and likewise, anaemia will not cause severe acidaemia.

      The other buffers are:
      Bicarbonate – carbonic acid – Carbon dioxide
      Phosphate
      Ammonia – Ammonium

      The last two are fine tuning, the bicarbonate buffer is the most important clinically. Carbon dioxide is removed easily by the lungs, so any excess in the system should be removed by healthy lungs. If the lungs are not healthy, or the lungs become overwhelmed, the excess CO2 cannot be ‘blown off’ and the buffer equilibrium moves to the left, and acidaemia results. Hence metabolic acidosis becomes acidaemia more rapidly in those with poor ventilatory function.

      Happy to chat about this difficult topic in person, if you wish.

  19. Polly Says:

    Hello,

    I’m just reading that ‘blue bloaters’ rely on hypoxic drive – obviously this means we can’t give them too much oxygen. However, what about ‘pink puffers’ – can we give them high oxygen levels?

    • dundeechest Says:

      Hi Polly,

      It’s not as straightforward as that, unfortunately. Whether or not a patient will retain CO2, and consequently have chronic type 2 respiratory failure, depends on more than “blue” or “pink”. The Blue Bloater / Pink Puffer distinction is how the patients cope with hypoxia – pink puffers increase their respiratory rate, keeping O2 up, and, mostly, CO2 down; blue bloaters do not increase their respiratory drive to lower their CO2, so they remain hypoxaemic, and develop the consequences of chronic type 2 respiratory failure, namely Cor Pulmonale.

      The bit that doesn’t fit is that there are plenty of cachexic patients who retain CO2, and plenty of bloated patients who do not. The only way to tell is someone has chronic type 2 respiratory failure is to do a blood gas – a high CO2 and a high HCO3 shows that the patient has chronic type 2 respiratory failure, and should receive controlled oxygen therapy aiming for SaO2 88 – 92 %. A normal bicarbonate is reassuring, and the patient can have controlled oxygen aiming for SaO2 94 – 98 %. Before the blood gas is taken it should be assumed that the patient has chronic type 2 respiratory failure, and SaO2 targetted at 88 – 92 %.

      Hypoxic drive alone does not explain CO2 retention in acute on chronic type 2 respiratory failure – you also need to think about V/Q mismatching. I wrote a response to a similar question earlier in the week, and here it is, reproduced for you:

      OK. Hypoxic drive.

      There are three drives to respiration: stretch receptors; hypercarbia; and hypoxia.

      The first is stretch receptors – if the lungs do not move, the stretch receptors do not fire, and we have the sensation of being short of breath. Hold your breath, as if you were underwater – you can do that for about 40 seconds before you really can’t suppress the desire to breathe. If you have a sats probe on your finger while you hold your breath, the sats will not fall; likewise if you have a CO2 probe on, the level does not rise; so the drive to breath comes from not breathing (!). You can over-ride this with practice, so you can train yourself to swim further underwater.

      The second, and important in COPD and other forms of Chronic Type 2 respiratory failure, is hypercarbia. There are chemoceptors in the brain that respond to elevated levels of CO2, as the levels rise, there is increased stimulus to breathe. If I put you into a box, let you breathe through a circuit in which the CO2 is removed (Carbonate pellets), and slowly reduce your oxygen levels, you would not increase your respiratory rate for some time; but if I let your CO2 levels rise in the closed circuit, but top up the oxygen levels to keep them normal, your respiratory rate increases dramatically. People with type 2 respiratory failure have a chronically high CO2 – the chemoceptors reset their baseline, so high CO2 levels do not stimulate an increase in respiratory rate.

      This leaves the third drive to breathe, hypoxia. The theory goes like this: in a normal individual, during respiratory failure CO2 will rise and O2 will fall: the rise in CO2 leads to an increase in respiratory rate, which keeps brings up the O2 levels. In a patient with chronic type 2 failure, during an acute event, the patient will not increase their respiratory rate in response to an increasing CO2, so they rely on having low O2 levels to stimulate their breathing. If patients are therefore given too much oxygen, they are no longer hypoxaemic, and therefore have “lost their hypoxic drive”, and no stimulus to breathe, thus their CO2 rises when given too much oxygen So the theory goes. And that is the core knowledge, and I suppose is the learning objective for this bit.

      There is more to it than that, though. If you want to read more about a more detailed explanation for why patients with chronic type 2 respiratory failure retain CO2 when given too much oxygen, click the tag for V/Q Mismatch, or just click here.

      This is a difficult concept, I think the most difficult to get to grips with out of the whole block. I will talk more about this on Wednesday, during the core clinical problems session

  20. Marge Says:

    The Glossary of Terms for Week 1 (page 8 of the study guide) stops in the middle of a sentence. The last entry is Antileukotrine – are we just missing the end of that entry, or is there more gone astray?

  21. Josh Scales Says:

    Hi,
    I hope you feel better
    Is there still an opportunity to come to the meeting with the respiratory gang and the radiology crew.
    On a sour note, my friend came back from the congo and he confirmed that they don’t drink umbongo there.

    • dundeechest Says:

      Feeling much better, thank you.

      If you are referring to the Tuesday morning Radiology meeting, you are all welcome to come along, every week.

      The lung cancer MDT is a busy meeting with little space, but you are welcome to come along: you might be turned away if there’s not enough space, tough.

  22. Medical Student Says:

    Hi, I was just wondering if there was meant to be a week 2 formative that we had to do – I tried to find one and couldn’t, and neither could the people I asked. I’ve read some of the, ahem, ranting, on here from other people to try and work it out and it seems maybe that there should have been 22 questions over weeks one and two and we got them all in week one? Maybe? I’m sure the answer is probably somewhere but I’m doing pretty well for me just being on the blog and reading some things (not the most technically minded of people and blogging and such like confuses me…).

    On another note, I’m repeating the year and there does seem to be a lot more enthusiasm for teaching now that this blog exists, perhaps because staff and students can actually interact directly and not have to do the scary thing of finding out someones email address to ask them a question that you possibly should already know the answer to bla bla bla…? Anyway, all the stuff we got last year is still going on, just with more opportunities for getting in touch and certain lecturers seeming more involved and like they actually care whether we get it. Not that anyone was bad last year. Just seems “better good” this year if that makes sense??

    • dundeechest Says:

      Hi

      There was meant to be a week 2 formative, and indeed there is one. It’s being uploaded just now, so you’ll be able to have a look at it later this week. We’ll post when it’s ready.

      The week 3 formative should be up well in time…

      Thanks for the comment on the teaching structure. As I mention in the course guide, we’ve always been happy that the course content has been fine, but the manner in which we deliver it has been not up to modern standards. I hope that I’ve managed to instil some enthusiasm into the teaching block, and provide some alternative resources to help you out. There’s more to come – watch this space.

      The other blocks have plans too – check out the other blogs….

  23. Josh Scales Says:

    Blood gas patterns from your fine lecture today slide 49

    o pH low, pCO2 high and HCO3 normal/ low = met acids
    o pH low, pCO2 v high and high HCO3 = resp acidosis
    o pH norm, pCO2 low and HCO3 norm – not a pH change and don’t know pO2 so what this fiddle sticks is going on?
    o pH norm, pCO2 high and HCO3 high – respiratory failure? But don’t know which type because don’t know O2

    Have I missed the point and I am indeed as stupid as my teachers told me when I was 14.

    Many thanks

    J-bone

    • dundeechest Says:

      pH low, pCO2 high & HCO3 normal/low = acute respiratory acidosis.
      pH low, pCO2 v high and high HCO3 = acute on chronic respiratory acidosis
      pH norm, pCO2 low and HCO3 norm = this is hyperventilation, to some degree, without pH change. This is typical of primary hypoxaemia, or type 1 respiratory failure
      pH norm, pCO2 high and HCO3 high = chronic respiratory acidosis, compensated type 2 respiratory failure

      You don’t need to know the pO2!

  24. josh Says:

    Is there any chance we could get Dr Andersons lecture powerpoint slides from today on blackboard please?
    Josh

  25. Asimo Says:

    hello!
    I’ve tried in vain to access two lectures…

    Friday 2nd October – ‘pathology of pulmonary vascular and pleural disease’ by FA Carey. It comes up with an error saying the text converter type is not installed. I think other students have had the same problem… it just doesn’t open up!

    Thursday 1st October- ‘clinical aspects of pleural disease’ by AW Anderson. I don’t think this slide has been uploaded yet.

    Any help would be great…
    Cheers in advance!

  26. laura Says:

    Hi Dundee Chest,

    Just completed the week 2 formative and got on ok up to question 37 and 38. I know that you have already explained the answers underneath each – but could you explain them a little further so that dozy here might catch on?

    For 37 – I answered cardiomegaly + pulmonary oedema.
    38 – I answered enlarged right ventricle with tricuspid regurgitation and normal left ventricle.

    I dont understand 38 in particular. I answered with an enlarged right ventricle – as in my thinking cor pulmonale is Right sided heart failure? ( He has a raised JVP and RV heave? )
    Am i being dim – or is the marking wrong?

    Thank you,
    Laura

    • dundeechest Says:

      OK.

      The first thing is Q38 – you’re right, and the marking scheme is wrong. I’ll ask the campus folk to change the marking.

      Q37 – if the patient has right heart failure the back pressure leads to peripheral oedema, raised JVP and pulsatile liver. The lungs have no increased venous pressure, unlike in LEFT ventricular failure when the back pressure leads to pulmonary venous hypertension, and pulmonary oedema.

      Sorry about Q38 having the wrong answer, we will sort that out.

  27. josh Says:

    Word up Dr T-Dog,

    Could you keep all the formatives up as they are a great and good to look back on as we reinforce our learning, I have spoken to others and they agree? I know its bank holiday and you have probably scived off but Dr Andersons slides still haven’t been uploaded, I don’t want to become a doctor and see a patient when I have no idea what is happening because I never saw Dr Andersons slides.

    Cheers

    Josh

    • dundeechest Says:

      I have passed on the request for Dr Anderson’s slides, I’m not sure about the hold up.

      The formatives should all go back up and stay up once the block is finished. Somewhere.

      Yes, I am having the day off!

    • Dundee e-MedEd Says:

      Hi Josh – I’ve now got Dr Anderson’s slides and have put them up in Blackboard.

  28. Sarah Macpherson Says:

    I didn’t understand the abbreviations in slide 43 of Dr. Winter’s lecture this morning about treatments of TB. The slide reads

    “2 months daily HRP and E or S – followed by 4 months HR”

    What does HRP and HR stand for? Is E ethambutol and S streptomycin? Thanks

    • dundeechest Says:

      I’ll ask William to comment on this later. But in the mean time:

      2 months of Rifampicin, Isoniazid and Pyrazinamide + Ethambutol or Streptomycin (We don’t really use much Streptomycin, to be honest)

      4 months of Rifampicin and Isoniazid.

      Who knows why there’s funny letters.

  29. Josh Scales Says:

    Dear Doc T-Bone Steak,

    I don’t want the respiratory block to end its been great.

    I have attached a table to an email, its probably rubbish but see what you think.

    Many thanks

    Peace out

    J-rex

    • dundeechest Says:

      You’re potty Josh.

      I have the table, I’ll post it up a wee bit later, thanks.

      The Resp block will end, but DundeeChestBlog will live forever!!!!

  30. Shereen Says:

    Hello, didn’t really know where else to say this but Group B had pathology tutorials today but we (groups B3 and B4) did not have a tutor, whereas the rest of B had a tutor as well as printed answers to the questions…

    We managed to pick what was left of the answer sheets from the other group after finding out that they had them. Most of the group don’t have answers and some of us would have appreciated a tutor as we learn better this way.

    • dundeechest Says:

      Sorry about that. One of the few things over which I have no control is the pathology sessions. I will ask the relevant parties, though, and try to get you an answer.

      It has become clear that the thing most of you want, most of the time, is tutor facilitated small group teaching. I will certainly be trying to organise that aspect of things more in the future.

  31. Sarah Macpherson Says:

    In the resp study guide on pg 7, the last question asks about the rationale for using ipratropium in combination with a beta 2 agonist and a glucocorticoid in asthma treatment. I’ve tried the bnf but wasnt getting anywhere. Could someone explain this please?
    Thanks

  32. Marge Says:

    Another pathology tutorial complaint/question! We (A1&A2) didn’t get a tutor for our tutorial either, and when someone went to the medical school office to check we were told that we hadn’t been scheduled to have a tutor. I think we’re all a bit dischuffed that some people have had the benefit of small group tuition and others haven’t. I know you’ve said above that you don’t have control over this, but I suspect that All-Powerful Consultants complaining has a bit more weight than mere medical students 🙂

    The question part – would it be possible to get the answers to the pathology tutorial? We had a look at the questions as a group, and we were ok with most of them, but I think there were a couple where we were unsure.


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