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TSR Med Students' Society Part VI

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Finally finished my surgical placement... My 8 weeks as a PA with cannulation skills is over until F1!
Done no work for finals and my PSA is soon, also why is it taking FPAS so so so long to tell us where we are living, it's getting rather annoying now
Original post by lcsurfer
Finally finished my surgical placement... My 8 weeks as a PA with cannulation skills is over until F1!
Done no work for finals and my PSA is soon, also why is it taking FPAS so so so long to tell us where we are living, it's getting rather annoying now


I think FPAS results are out 9th of March, so still a few weeks yet.

Original post by nexttime

Also apparently furosemide has evidence in acute pulmonary oedema, but not as part of routine therapy.


Yeah, SOD OFF is the acronym for flash pulmonary oedema - sit up, oxygen, diamorphine (reduce SOB), OFFLOAD (furosemide 80mg)
Loop diuretics don't actually improve mortality in HF patients though, they relieve symptoms so are on repeat script but patients often don't adhere as the polyuria is a bugger.
Mortality reduction Tx in HF are ACE-i, Beta Blockers, K+sparing diuretics, hydralazine and nitrates (I think there is evidence for these two re-mortality).
Digoxin can also be used to increase force of contractility (positive inotrope), but again this is just symptomatic relief.

Also just as an add-on to the drug revision list above I remember I SLAVE for COPD/most chronic resp. treatments - Inhalers, Stop smoking, Long-term OT, Abx, Vaccines, Exercise (+/- chest physio + drainage)
Hi! I’ve been working with this person and I’m really puzzled about something they told me. Google wasn’t helpful so I decided to ask you guys instead.

This person has a genetic disorder that affects collagen production. Some years ago they were in intensive care because they had sepsis. The resulting muscle weakness got better with time, but their breathing never did. They had had some breathing problems before the hospital episode but this was much worse and they have been using supplemental oxygen ever since.

Apparently doctors told them that they couldn’t breathe properly because the inflammatory response had damaged the “hairs or vesicles or something”. (Alveoli are called lung vesicles in my language.) The person said that the things had “fallen flat and not gotten up, and they never grow back”. They showed me this grass-falling-down-in-the-wind-imitating movement so I assumed they meant cilia.

I found out on the internet that sometimes being in a ventilator can cause “biotrauma” so the inflammatory response part could make sense. When I realised that the person meant cilia I asked whether they had had a cough, and they said that they hadn’t and it had actually really puzzled their doctors as well. They said that they don’t get mucus in their lungs (is this possible??), and even though they have to blow in a bottle every week to remove excess mucus they said that it has no effect on them. I can only think of one way in which cilia damage could cause breathing trouble and that’s the accumulation of too much mucus, but I suppose that’s not what happens if they never had a cough and the bottle thing doesn’t help. Biotrauma apparently affects alveoli instead of cilia which would make more sense symptom-wise. I was thinking that maybe the collagen thing could make it even harder for the alveoli to regain elasticity after they’ve been damaged? If that’s the case I don’t understand why they and their doctors seemed to talk about cilia, why the person seemed to know a lot about mucus and was sure that the damaged parts are supposed to transport mucus out of the lungs, and why they have to blow in the bottle though.

Does anyone know what’s actually going on here?
Original post by StationToStation
Hi! I’ve been working with this person and I’m really puzzled about something they told me. Google wasn’t helpful so I decided to ask you guys instead.

This person has a genetic disorder that affects collagen production. Some years ago they were in intensive care because they had sepsis. The resulting muscle weakness got better with time, but their breathing never did. They had had some breathing problems before the hospital episode but this was much worse and they have been using supplemental oxygen ever since.

Apparently doctors told them that they couldn’t breathe properly because the inflammatory response had damaged the “hairs or vesicles or something”. (Alveoli are called lung vesicles in my language.) The person said that the things had “fallen flat and not gotten up, and they never grow back”. They showed me this grass-falling-down-in-the-wind-imitating movement so I assumed they meant cilia.

I found out on the internet that sometimes being in a ventilator can cause “biotrauma” so the inflammatory response part could make sense. When I realised that the person meant cilia I asked whether they had had a cough, and they said that they hadn’t and it had actually really puzzled their doctors as well. They said that they don’t get mucus in their lungs (is this possible??), and even though they have to blow in a bottle every week to remove excess mucus they said that it has no effect on them. I can only think of one way in which cilia damage could cause breathing trouble and that’s the accumulation of too much mucus, but I suppose that’s not what happens if they never had a cough and the bottle thing doesn’t help. Biotrauma apparently affects alveoli instead of cilia which would make more sense symptom-wise. I was thinking that maybe the collagen thing could make it even harder for the alveoli to regain elasticity after they’ve been damaged? If that’s the case I don’t understand why they and their doctors seemed to talk about cilia, why the person seemed to know a lot about mucus and was sure that the damaged parts are supposed to transport mucus out of the lungs, and why they have to blow in the bottle though.

Does anyone know what’s actually going on here?


Possibly if he's got muscle weakening, might he be unable to clear the mucous, thus maybe he lacks the coughing reflex? Can't imagine how that would work without him choking. No idea.
Original post by That Bearded Man
Possibly if he's got muscle weakening, might he be unable to clear the mucous, thus maybe he lacks the coughing reflex? Can't imagine how that would work without him choking. No idea.


Thought about this too but I've heard them cough once when they tried to drink and it went down the wrong way, so I don't think it's that :s-smilie:
Original post by StationToStation
Does anyone know what’s actually going on here?


Excessive mucus production is very nonspecific and pretty common in chronic lung diseases. Clearing mucus is dependent on cilia but also good air flow, good lung elasticity and a good cough. Problems clearing it are common in diseases processes like COPD, asthma, CF and at the end of life.

This case is interesting though - doesn't sound like they have a major problem and they don't seem to be coming down with frequent infections, a hallmark of improper mucus clearance. So maybe theirs is really mild.

There are a few different collagen disorders that could meet that description, and I don't know much about them. In any case, post-ventilator problems are pretty niche and I wonder whether me looking them up will help much!

My only theory would be: collagen disorder predisposes to alveolar breakdown, and the sepsis/ARDS caused significant alveolar damage and bulla formation - emphysema basically.

But I have no idea whether that's true - significant fibrosis or neuromuscular weakness are two other quite possible causes.

So to answer your question: no, no idea.

Original post by StationToStation
Thought about this too but I've heard them cough once when they tried to drink and it went down the wrong way, so I don't think it's that :s-smilie:


Interesting that happened - aspiration is a sign of muscular weakness/malcoordination. Wonder if it's related.

Also interesting that they had a significant bout of sepsis - hardly a common occurrence and makes me wonder if either a) immunocompromise is part of their disease or b) they take immunosuppressants as treatment, in which case it isn't hereditary - just autoimmune (sometimes patients mistake the two).
(edited 7 years ago)
Original post by nexttime
Excessive mucus production is very nonspecific and pretty common in chronic lung diseases. Clearing mucus is dependent on cilia but also good air flow, good lung elasticity and a good cough. Problems clearing it are common in diseases processes like COPD, asthma, CF and at the end of life.

This case is interesting though - doesn't sound like they have a major problem and they don't seem to be coming down with frequent infections, a hallmark of improper mucus clearance. So maybe theirs is really mild.

There are a few different collagen disorders that could meet that description, and I don't know much about them. In any case, post-ventilator problems are pretty niche and I wonder whether me looking them up will help much!

My only theory would be: collagen disorder predisposes to alveolar breakdown, and the sepsis/ARDS caused significant alveolar damage and bulla formation - emphysema basically.

But I have no idea whether that's true - significant fibrosis or neuromuscular weakness are two other quite possible causes.

So to answer your question: no, no idea.



Interesting that happened - aspiration is a sign of muscular weakness/malcoordination. Wonder if it's related.

Also interesting that they had a significant bout of sepsis - hardly a common occurrence and makes me wonder if either a) immunocompromise is part of their disease or b) they take immunosuppressants as treatment, in which case it isn't hereditary - just autoimmune (sometimes patients mistake the two).


This person has a rare, dominant disorder called osteogenesis imperfecta. It's definitely genetic although I think most cases, including theirs, are sporadic? Don't know if these things are relevant but here's the rest of what I know:
- The person is really short. Their bones break really easily and they have had over 30 fractures.
- They said that because of their scoliosis their lungs are pushed towards the abdomen so apparently the breathing situation is getting progressively worse as the lungs have less and less space. This is happening slowly though - as I said things got from almost normal to requiring supplemented oxygen after they were in the hospital for a while.
- If I remember correctly the sepsis was caused by a urinary tract infection...? Also, when they finally went to the hospital about this they had a really high fever and were put in the ICU almost straight away.
- They had a heart attack when they were pretty young even though they live quite healthily
- They have a high blood pressure and have developed mild pulmonary edema many times
- Sleep apnea is common in this disorder although nobody knows why - it's being researched atm. The person suffered from it until they started using this ventilator type thing at night.

Yep alveolar damage is my best guess too (although obviously I don't know very much about this stuff). Is there something special about respiratory muscles with regards to neuromuscular weakness? They told me that when they started getting better in the hospital they weren't even able to press phone buttons or anything but they got their strength back a long time ago - I think this hospital episode was like 5-10 years ago - so at least to me it sounds pretty weird that their lungs wouldn't have recovered in the same way?

It could be that they're immunocompromised too yeah. I guess that a problem with collagen would affect pretty much everything in some way.

Thanks for the answer!!
(edited 7 years ago)
Original post by BrillliantModest
I think FPAS results are out 9th of March, so still a few weeks yet.



Yeah, SOD OFF is the acronym for flash pulmonary oedema - sit up, oxygen, diamorphine (reduce SOB), OFFLOAD (furosemide 80mg)
Loop diuretics don't actually improve mortality in HF patients though, they relieve symptoms so are on repeat script but patients often don't adhere as the polyuria is a bugger.
Mortality reduction Tx in HF are ACE-i, Beta Blockers, K+sparing diuretics, hydralazine and nitrates (I think there is evidence for these two re-mortality).
Digoxin can also be used to increase force of contractility (positive inotrope), but again this is just symptomatic relief.

Also just as an add-on to the drug revision list above I remember I SLAVE for COPD/most chronic resp. treatments - Inhalers, Stop smoking, Long-term OT, Abx, Vaccines, Exercise (+/- chest physio + drainage)


We use PODMAN for acute pulmonary oedema
Position (sit upright)
Oxygen
Diuretics
Morphine
Anti-emetics
Nitrates

I think it's from the OSCE stop website
So, CMT is two years of hospital posts.
GPVST is 1.5+1.5 of hospital + GP.

Am i correct in that even if you did CMT (or ACCS-AM), you'd have to repeat the 1.5 of hospital posts if you switch to GP training?

It seems like the silliest requirement if that's the case :s
Original post by hslakaal
So, CMT is two years of hospital posts.
GPVST is 1.5+1.5 of hospital + GP.

Am i correct in that even if you did CMT (or ACCS-AM), you'd have to repeat the 1.5 of hospital posts if you switch to GP training?

It seems like the silliest requirement if that's the case :s


Different hospital posts though - CMT posts are all in general medical specialties, whereas in GP whilst you may get a rotation in general medicine, you'll rotate through other things such as paeds, gynae, psych, A+E and surgical specialties.

Posted from TSR Mobile
Original post by Mushi_master
Different hospital posts though - CMT posts are all in general medical specialties, whereas in GP whilst you may get a rotation in general medicine, you'll rotate through other things such as paeds, gynae, psych, A+E and surgical specialties.

Posted from TSR Mobile


Ah right. Makes more sense. Thanks :biggrin:
Question ...(exam panic so forgive me if its something I should know).

Spinal anaesthetics and the spaces they go in to? Can someone talk me through it, specifically the anatomy of these spaces.

Thank ye in advance

@Helenia I'm guessing you will know (I hope you don't mind the tag).

I have googled this but I am really bad at visualising spaces/anatomy and my head is rather ****ed atm.
A spinal needle is inserted into the L2/3 L3/4 L4/5 or L5/S1 interspace. The tip enters the subarachnoid space and this is where the local anaesthetic is delivered. The reason that they're put in at these levels is that the spinal cord terminates at L1 in an adult and therefore you're at low risk of hitting the spinal cord and causing direct trauma to it at this level.

Usually hyperbaric bupivacaine is used (+/- opioid) and the basicity allows the level of spread of the local anaesthetic to be controlled by changing the patient's position. Search youtube for "the glass spine" for a useful video that illustrated this.
Original post by ForestCat
Question ...(exam panic so forgive me if its something I should know).

Spinal anaesthetics and the spaces they go in to? Can someone talk me through it, specifically the anatomy of these spaces.

Thank ye in advance

@Helenia I'm guessing you will know (I hope you don't mind the tag).

I have googled this but I am really bad at visualising spaces/anatomy and my head is rather ****ed atm.


A spinal anaesthetic is also known as a sub-arachnoid block, so the needle goes through the dura and arachnoid mater, and local anaesthetic is injected into the CSF (you confirm position of your needle by seeing CSF come back through it). As SW says, any of the spaces from L2/3 down to L5/S1 can be used - classically you are aiming for L3/4, but in reality the surface anatomy is variable so you can't actually be sure that's the one you're hitting. Spinals tend to be a single shot injection of low volume, relatively high concentration local anaesthetic, and will provide surgical anaesthesia for ~2 hours, but it will take several more hours for a full return to function.

An epidural is inserted into the epidural space - outside the dura. You do NOT want to see CSF in your needle when putting one of those in! You can do a single shot injection here, but far more commonly a catheter is introduced into the space and the drug infused continuously (or as a basal-bolus regime) down the catheter. Epidurals can be used with a high volume, low concentration mixture both for analgesia in labour or post-op, or can be topped up with more concentrated LA for surgery. HTH!

Original post by Spencer Wells
x.


Original post by Helenia
x





Thank you both!!!
Question (mainly) for females student/doctors:
is it acceptable to wear make up during placements? I don't mean fancy smokey eyes and red lipstick, but more like a bit of mascara and some "natural" eye shadow/lipstick.
I never really wore make up before (still use the same mascara I bought when I was 15), but I recently realised I actually feel much better with a bit of eye make up. However, I don't want to risk any disciplinary issues when I start CP1 in a week time
Original post by Nottie
Question (mainly) for females student/doctors:
is it acceptable to wear make up during placements? I don't mean fancy smokey eyes and red lipstick, but more like a bit of mascara and some "natural" eye shadow/lipstick.
I never really wore make up before (still use the same mascara I bought when I was 15), but I recently realised I actually feel much better with a bit of eye make up. However, I don't want to risk any disciplinary issues when I start CP1 in a week time


A few female students were spoken to in Derby informally, but it was a combination of clothes and hair being down more than make-up.

Posted from TSR Mobile
Original post by Nottie
Question (mainly) for females student/doctors:
is it acceptable to wear make up during placements? I don't mean fancy smokey eyes and red lipstick, but more like a bit of mascara and some "natural" eye shadow/lipstick.
I never really wore make up before (still use the same mascara I bought when I was 15), but I recently realised I actually feel much better with a bit of eye make up. However, I don't want to risk any disciplinary issues when I start CP1 in a week time


That's fine:smile:
At mines, they stress no short skirts (I.e above knee) and hair tied back if it's long and for guys to iron their shirt :tongue:
Original post by Nottie
Question (mainly) for females student/doctors:
is it acceptable to wear make up during placements? I don't mean fancy smokey eyes and red lipstick, but more like a bit of mascara and some "natural" eye shadow/lipstick.
I never really wore make up before (still use the same mascara I bought when I was 15), but I recently realised I actually feel much better with a bit of eye make up. However, I don't want to risk any disciplinary issues when I start CP1 in a week time


Makeup is fine. I'll have a bit of a flick of eyeliner on most days, honestly and I've worn a slightly brighter lip before. If it's work appropriate and it won't offend anyone there's no issues.

Just don't turn up in false eyelashes, that's the only thing that's well and truly banned for infection control reasons. And please don't use mascara that's over 6 months old! :eek:
Original post by Helenia
A spinal anaesthetic is also known as a sub-arachnoid block, so the needle goes through the dura and arachnoid mater, and local anaesthetic is injected into the CSF (you confirm position of your needle by seeing CSF come back through it). As SW says, any of the spaces from L2/3 down to L5/S1 can be used - classically you are aiming for L3/4, but in reality the surface anatomy is variable so you can't actually be sure that's the one you're hitting. Spinals tend to be a single shot injection of low volume, relatively high concentration local anaesthetic, and will provide surgical anaesthesia for ~2 hours, but it will take several more hours for a full return to function.

An epidural is inserted into the epidural space - outside the dura. You do NOT want to see CSF in your needle when putting one of those in! You can do a single shot injection here, but far more commonly a catheter is introduced into the space and the drug infused continuously (or as a basal-bolus regime) down the catheter. Epidurals can be used with a high volume, low concentration mixture both for analgesia in labour or post-op, or can be topped up with more concentrated LA for surgery. HTH!



Just another few quick questions to add on if you dont mind!

what are the main differences between both needles except gauge size?
and how long can the epidural catheter remain before it has to be removed?

Thanks alot!

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