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”
…this is a blog by Kal, one of the edinburgh paramedics. his latest post of a guy in DKA explains DKA and diabetes and acidosis really well in an amusing and ‘idiot proof’ way. well, i think so anyway. thought the 2nd years might enjoy in the run up to exams….might shed some light on something i know i had issues with. Hx
Where is this blog of which you speak….?
Hey,
wondering if there was anychance of a couple more formative assessments for the last 2 weeks of respiratory? The first two are really useful as it gives explanations to why each other option isn’t right instead of just going WRONG. Also if you could mention it to the other system convenors at the next big meet or pub crawl i’d be very grateful cause i find it kinda stange that they’ve just adandoned them. Every system had them in first year and they were ridiculously good for showing you how little you actually knew.
We have formative assessments for all 4 weeks. I can make them accessible on the site, but they will need a re-write for the formatiing.
Bear with me a wee while.
Hello,
Could you clarify the difference/relationship between lung collapse, pneumothorax and tension pneumothorax?
Looking forward to the formative assessments.
Pneumothorax is air within the thoracic cavity. A whole in the visceral pleura allows air to escape from the lung, into the pleural space. The build up of air in the pleural space compresses the lung, or the air passes directly through the whole into the pleural space, rather than inflating the lung.
A tension pneumothorax is a pneumothorax in which the air enters the pleural cavity but cannot escape, so as more air enters, the pressure increases. Once the pressure is high enough, the SVC and IVC become compressed, and venous return is compromised. This is a life threatening complication.
Lung collapse is due to an obstruction of the airway. The pleura is not breached. When the airway is obstructed, the distal lung collapses, as it is not aerated. As the lung collapses, the total lung volume decreases leading to the hallmark sign on lobar collapse – one lung big. one lung small.
This is a question going back to the first week of respiratory. Respiratory revision has begun for me and I’m pretty unsure about the answer to one of the questions in the study guide
The question is “Is airway resistance constant during the inspiratory cycle? Expand your answer.”
I believe the answer is no, however, I’m not entirely sure why. I believe it is to do with negative pressure in the airways causing them to compress down, narrowing them, and increasing resistance during expiration. I’ve just got a picture in my mind with arrows pushing down on a virtual alveolus and a virtual little airway. Does this make any sense?
Thanks in advance for any help!
Give me a couple of minutes to answer that one….
Hi, what’s the difference (if any) between granulomatous alveolitis and sarcoidosis alveolitis…? thanks!
actually that was a silly questions
question*
Hi,
Is Farmer’s Lung classified as a type III or type IV hypersensitivity reaction? I know that it involves immune complex deposition but apparently it is also granulomatous (foreign bodies)?
thanks
In answer to Amy,
Farmer’s lung is an example of extrinsic allergic alveolitis. In Dr. Fardon’s immunology of hypersensitivity reactions farmer’s lung is described as an “in situ type III hypersensitivity.” The immune response is to the mould. As said on Dr. Fardon’s 52nd slide (p. 65 on the pdf) the type III hypersensitivity is due to antibody-antigen deposition. Type IV hypersensitivity (resulting in granuloma formation) arises because of the inability to clear the immune complexes.
This means that farmer’s lung has both the mechanisms of type III and type IV hypersensitivity.
Hopefully this makes sense…
If I’m getting it wrong, let me know!
See the answer from Pierre R – he’s spot on with his answer.
It’s a combination of both III and IV
Would you be able to explain the difference between types 1 and 2 respiratory failure and the pink puffers and blue bloaters?Books are very unclear about this!
OK. This is the question I get asked about the most, the concept people get wrong most often, and is consistently poorly understood.
Type 1 respiratory failure is hypoxaemia. The pO2 is low, the pCO2 may be low (due to hyper-ventilation to compensate for hypoxaemia) or normal.
Acute type 2 respiratory failure is hypoxaemia with hypercarbia. The pO2 is low, the pCO2 is high. pH is usually low. This follows type 1 failure, usually because of exhaustion, and consequent hypoventilation.
Chronic type 2 respiratory failure is hypoxaemia, long standing hypercarbia with metabolic compensation. The pO2 is low, the pCO2 is high, the HCO3 is high. pH is normal. This can occur in any disease that causes chronic hypoventilation.
Acute on chronic type 2 respiratory failure is hypoxaemia, long standing hypercarbia with metabolic compensation, and an acute event leading to a further hypercarbia, and consequently, acidaemia. The pO2 is low, the pCO2 is very high, HCO3 is high, the pH is low. Think acute exacerbation of any cause of chronic type 2 respiratory failure.
Fotget blue bloaters and pink puffers, the concept is not useful, to my mind.
Thanks, that makes much more sense now!
thanks pierre!
DC : in asthma, can you explain the order of drugs used, I don’t really understand the circumstances for using ACh antagonists, is it just in acute asthma these are given?thanks
Hi DC,
Just been looking over asthma.
Out of interest, with all the available investigations I wondered what you really use in practice. The clinical picture is obviously really valuable and in most cases goes a long way to telling you the diagnosis however, when your stuck…what do you choose and why? I know you’d start with cheapest and least invasive, of course!
I know a PEFR diary is helpful in that it may show diurnal variability and with spirometry you will likely see an obstructive pattern. CRX is usually normal and skins allergen tests may be useful. But would you necessarilly carry out histamine provocation tests, for example?
Thanks
hey
where is that video of the breath sounds?
i have looked but its not in the resource??
cheers
@Stewart – I’ll put it up later this afternoon. I’ve been teaching all day, so no time to upload it.
It’s on the old DC1 site (http://dundeechest.wordpress.com)
Hi – I’m struggling to comprehend the management of acute asthma. I was just looking in a textbook and at the BTS Guidelines management of acute asthma – but I’m still a little confused.
What do you give and in what order and how much?
I know you give O2 to maintain sats at 94-98% and nebulised Salbutamol – but how much? What is the dose for Ipratropium? – Inregards to steroids again BTS simply mentions “Give steroids in adequate doses in all cases of acute asthma. Continue Pred. 40-50mg daily for at least 5/7 or until recovery” – what is the starting dose? and what is the clinical indication/point at which IV magnesium is considered?
Is there a Tayside Protocol? I’m sure there must be one, but I can’t find it.
Thanks – I’m probably confused over something really simple, but I’d really appreciate the clarification as I don’t want to mistreat a patient one day!
Thank you for clarifying the managment of acute asthma for me!
Ipratropium used or not really? – if so how much.
Thanks again.
Hi,
Do we need to know the side effects of the TB drugs…at this stage?
thanks!
@ Amy. Yes it is important to understand the side effects of AntiTuberculous chemotherapy, would you like me to write a short post about it on the site?
Thank you very much, that is very helpful.
Hello DC,
Was just going through the lecture you gave in week 4 with poor little suzi. I think I understand the blood gas results but I am getting confused between FiO2 and p02 and was wondering if you could please explain the difference. Thanks 🙂
FiO2 – Inspired oxygen concentration
pO2 – partial pressure of oxygen
Hope that helps.
I was wondering if you could please explain the answers to this question. Thank you.
OPTIONS:
A Nebulised salbutamol
F Oral prednisolone
B Oral theophylline
G Intravenous Aminophylline
C Oral salbutamol
H Intravenous doxapram
D Inhaled salmeterol
I 24% oxygen
E Inhaled beclomethasone
J 60% oxygen
For each of the following patients select the most appropriate treatment option.
7 A 70 year old male, heavy smoker, is admitted with wheezing and increasing breathlessness to the Accident and Emergency Department. He has already been given first-line bronchodilator therapy and is currently on a 28% inspired concentration of oxygen via a mask. His arterial blood gas analysis is as follows:
PaO2 KPa (normal > 12 KPa), SaO2 81% (normal > 95%), PaCO2 8.1 KPa (normal < 5.0 KPa),
pH 7.31 (normal 7.35-7.45), HCO3 32 mmol/l (normal range 22-26 mmol/l).
You decide to increase his inspired oxygen concentration from 28% to 35%. What other drug should you also add-in at this juncture?
8 A 40 year old non-smoking woman presents to her GP with a history of increasing wheeze, particularly with night-time symptoms. She also has a history of allergic rhinitis. On examination she has bilateral wheezing in her chest with good air entry and her peak expiratory flow rate is 300 l/min (predicted normal 400 l/min). What preventative long-term therapy should you start this patient on?
9 A 25 year old male non-smoker is admitted with a history of increasing wheezing and breathlessness following a recent viral respiratory tract infection. Despite first-line bronchodilator therapy given on two occasions within the first 30 minutes of admission, he ihas not improved. His peak expiratory flow-rate is 100 l/min (predicted normal 570 l/min), respiratory rate 35 per minute, heart rate 120 per minute. He is now feeling tired and having difficulty completing sentences. What second-line bronchodilator therapy should you now administer?
7 H
8 E
9 G
Thank you. I don't understand. kx
@Kat Sure thing.
I don’t agree with answer 7. We very rarely use doxapram these days. It is a primary respiratory stimulant, so useful when patients have hypoventilation due to *low respiratory rate*. It does not say what his respiratory rate is, so I cannot recommend doxapram in this situation. I would give aminophylline in this situation, and wait for 1 hour, then consider NIV. I would also give parenteral steroid.
8. This patient has atopic asthma. First line preventative therapy is an inhaled corticosteroid, in this case beclomethasone.
9. This patient has post viral wheeze, probably due to un-diagnosed asthma. The question asks which second line bronchodilator you would use. The answer is ipratropium, but that isn’t an option. Of the other bronchodilators: nebulised salbutamol is the first line bronchodilator; oral theophyllines take too long to work; oral salbutamol is next to useless; salmeterol has a delayed onset of activity (about 30 mins) so it not appropriate; IV aminophylline works quickly. As I said in the revision lecture, the local protocol, based on the latest national guidance, is to give salbutamol and ipratropium, consider IV magnesium, then call an anaesthetist.
Where did you get these questions? I disagree with the first one, the second one is fine, the third one is out of date.
thank you! I got number 8 right -but I didn’t understand 7 or 9 (those are the answers we were given!) – thought we hadn’t been taught that – they were the questions Dr Day put on Blackboard as practice for our year 2 exams on Monday!! I hope there aren’t anymore out of date questions in the actual exam!
btw – yes, put option H for q 7 and then for question 9 I too wanted to give Ipratropium – but it wasn’t answer so assumed he’d already been given neb. salbutamol and then opted for Theo. as then next best out of the options – was that daft?!!! thanks again.
woops i meant I put Amino. option “G” for question 7. thanks
Thanks DC. Oh dear I hope there aren’t either kat! But didn’t you say you wrote them DC so hopefully it will be OK? 🙂
The problem we have is that the bank of questions goes back a long way – a lot of what we tested 5, or 10 years ago is now out of date. Doxapram was widely used 10 years ago, but NIV works much better, and we now appreciate that V/Q matching is far more important than any concept of “hypoxic drive”.
The doxapram theory was that if you give more O2, the respiratory rate will fall, and the doxapram will counteract the fall. Resp rate doesn’t fall, it remains high, so dopram is of little use.
So for the exam questions – we write as many new questions as we can to replace out of date questions, and we try to make the questions less ambiguous, but it’s a very large task.
When we mark the questions we sometimes disagree with the mark scheme, and we sometimes allow “wrong” answers, if they fit modern practice.
This is meant to reassure you; I know it won’t very much, but try to trust us that we’re trying to pass you, not fail you, so we are on your side.
@Kat – Theophylline not totally daft, but it is an oral preparation, so takes quite a long time to be absorbed, and then reach the lung. Usually it takes about 5 days for oral theophylline to reach steady state.
Loading with IV aminophylline takes 30 mins (5mg per kg loading dose, 0.5mg per kg per hour thereafter)
cool – thanks – it was just that before I realised that the questions were totally out of date I remembered you saying something on Wednesday about IV aminophylline not being used in acute asthma but sometimes being used in acute exacerbation of COPD – is that right or have I got the wrong end of the stick? I’m sure someone shouted out a question about it at the lecture…. thanks again. 🙂
Hi there, was just wondering if you could clairfy what ARDS is?I have never quite grasped the concept of what happens in it or why you would get it. Thanks!
@Kat – you have it right. We frequently use aminophylline in COPD, but far less commonly in Asthma.
@Katie.
ARDS is the end stage of a variety of acute lung injuries. It is defined as an pO2/FiO2 > 200, a CXR with bilateral alveolar infiltrates, and a pulmonary artery wedge pressure of < 28 mm Hg. Essentially this means non-cardiogenic pulmonary oedema. Fluid leaks out of the interstitium, into the alveolar spaces. The fluid is protein rich, and causes severe respiratory failure. ARDS has a very high mortality (>70%), and is an ominous sign in any disease.
Ok thank you. This might be really stupid but can it be classified as etiher a type 1/2 respiratory failure? Also is there any treatment that can be given or if it is an end stage problem will the lungs already be too damaged?
It can be type 1 or type 2, depending on the severity, the duration, and the general condition of the patient. Patients with ARDS are usually intubated, or dead.
Treatment is low pressure ventilation, and supportive management.
ok thanks for clearing that up!
DC: do you know if our exam is negatively marked? cause I just did some questions – got 82%, not brilliant – but not awful, but if they were negatively marked I only got 64%!!!!! 🙁
@ Kat – it’s not negatively marked. Looks like you’re going to sail through the exam. Well done.
And good luck.
Not respiratory related but
I was wondering why prn seemed to be down at the moment?
If you know that is…
I think it’s transferring servers to the university run server just now…. Look for a speed increase when it transfers.
Hey DC,
Was looking through your SSC/4th year project section, and would really be interested in undertaking a respiritory SSC and/or audit at some point, was wondering how I go about arranging that? You mentioned on DundeePRN that you were looking for a couple of ‘keen’ students (guinea pigs?) for a project, and I think Issmael and I expressed interest but haven’t really heard anymore about that?
Currently a second year (awaiting resit exams, goody), but if you could maybe drop me an email on the matter?
Thanks,
Emily
Yes, there’s always things to do. The thing I mentioned on PRN has been taken on by two of the registrars, so you’ve missed out on that, but there’s plenty of other things to do. Best thing is just to pop down to the department and see me, then we can discuss what you want to do, long or short term project, that sort of thing.