#hyperkalaemia

[biology-geology-beaches-india]

TSRNOSS, p 531.

[neosciencehub]

AstraZeneca Receives Approval for Hyperkalaemia Treatment in India @neosciencehub #AstraZeneca #Hyperkalaemia #India #CDSCO #sodiumzirconiumCyclosilicate #neosciencehub

[hesi-teas-test]

HESI A2: Master Bio-chemistry with Real Exam Practice Questions

Practice Time Management

Each section has a time limit, so practice answering questions under timed conditions to help you manage your time effectively during the test.

What is the normal adult respiratory rate?

a) 12–20 breaths per minute

b) 18–24 breaths per minute

c) 10–15 breaths per minute

d) 16–28 breaths per minute

The correct answer is: a) 12–20 breaths per minute

For a normal adult at rest, the respiratory rate typically ranges from 12 to 20 breaths per minute. If the rate falls outside of this range, it may indicate an underlying health issue that needs further investigation.

A patient is prescribed a diuretic medication. Which of the following side effects should the nurse monitor for?

a) Hypokalaemia

b) Hypercalcemia

c) Hypertension

d) Bradycardia

The correct answer is:

a) Hypokalemia

Diuretic medications, particularly loop diuretics and thiazide diuretics, can lead to a decrease in potassium levels in the blood (hypokalemia) due to increased urine output. This is an important side effect to monitor for, as low potassium can cause symptoms like muscle weakness, cramping, and arrhythmias.

It's important to check the patient’s electrolyte levels and watch for any signs of imbalance. Potassium-sparing diuretics, on the other hand, are more likely to cause hyperkalaemia.

To get more questions and practice lesson you can download HESI Test Prep 2025. 👈

[ladymedic]

Hyperkalaemia ECG changes in 15 seconds. 

High levels of potassium destabilise the cardiac membrane causing arrhythmia’s which lead to cardiac arrest. This can be a real life-saving opportunity if you can catch and treat it!

I made this as an experiment while learning a bit more about After Effects to animate my medical illustration. Hope it’s useful!

[anattempttostudyharder-blog]

29/5/23 (Day 37)

Did a mock today

Solved questions in genetics and neurology

Wrote orthopaedic notes

Did a cardio workout

//Studied 6.5 hours today. The main issue with taking a mock is that I need to do it at the start of the day when I'm alert and awake. But sitting for a mock exhausts my brain so much, it's so hard to study later.//

Mock analysis (72 days left for PLAB)

Again good time management, i finished it within 2 hours

A lot of half baked knowledge in my head (for example there was a question about villous adenoma and ik that it presents with some abnormality of potassium in blood but I couldn't remember if it was hyperkalaemia or hypokalaemia and obviously both options were given)

Still cannot localise lesions in neurology because I never bothered to do a deep dive and study it

The good part was my scores did improve! I did want to score 140/180 (currently at 136) but hopefully next time I can meet that requirement and even go higher.

[idealisticrealism]

TCL 2x11 recap

Ok so in honour of the S3 renewal (!!!! shut up I’m not crying YOU’RE crying aaaaaaahhhh!!!) here are a few very very belated TCL thoughts… and of course, many many many more thoughts still to come for 2x12 lol 

So I am already immediately needing to know how much time has passed between last ep and this one lol. Maybe a few days? I mean Luca is looking so much better, and he’s so excited to see Fi and his cousins. (Lol at the fact Marco doesn't even get mentioned, even though he only died like 2 months ago. Like yaasss everybody, Marco who???). Also I really like the way Thony asks “JD let you come?”, bc it’s not judgmental or snarky, it’s more acknowledging the difficult position Fi is in and her gratitude that she came. Also oooh we are definitely back in Vegas for the filming now– this is filmed at Adventuredome in LV. But ugh Thony going from smiling at Luca’s excitement to spotting Joseph :( poor woman just can’t even get 5 minutes of simple happiness before something drags her back down again. (Also I assume she still has her big bald shadow following her around and so that’s how Joseph knew where to find her?) 

Oooh Nadia definitely still has her shadow. And damn she’s in the fanciest of prisons rn, stuck in RK’s penthouse. Since this phone conversation is apparently the first time she and Arman have talked since she poisoned RK, and Arman isn’t looking completely panicked about where she's been, then I’m guessing not too much time could have passed since then– maybe it really has only been a few days? Also I really wanna know how much Arman was able to find out about what happened to RK? Like did he finally hurry into Fast Lane after his little excursion with Garrett, frantically looking around  to see if Nadia might still be there, only to find all the staff gossiping about how the boss was taken to hospital and how Ms Morales went with him??? And then he tries to call her but can’t get through– so what did he do??  Did he text her and risk it being seen by RK, or did he just go home and sit there waiting by his phone? Also ugh I wish we got to see his reaction to her saying that Thony saved RK, bc yasss to that drama lol.  And ugh yes to Nadia referring to Thony as ‘your cleaning lady’ again.  Idc that Nadia means it in a negative way, it’s still implying a connection between Armony and that’s what I’m all about lol. Anyway I did like that Arman was immediately down to rescue Nadia though. Oh my sweet brave yet somewhat stupid boy lol. Also goddammit I really gotta learn spanish bc while I very much respect them not using subtitles a lot of the time, I still always wanna know everything that's being said lol

Haha RK is Big Mad about his heart attack. “I had a full physical just a few months ago, there was nothing that indicated any issue with my heart” ok well I mean a ‘physical’ is a pretty basic check, so unless the doctor randomly decided to arrange an angiogram (a surgical procedure which is not done on people who don’t have symptoms), then there’s no way they could have definitively known the heart was fine… so maybe calm down a bit there buddy? Also again, we saw last ep that you’re on blood thinners, so there is definitely something wrong somewhere.  But lol the hot doctor guy saying “high potassium can cause hyperkalaemia” is so funny because hyperkalaemia is literally just the technical term for high potassium. But props to him for telling RK it could have been caused by stress lol– you’re a brave and potentially foolish man, Doc. Also loooolllll RK pouting in the bed like a petulant child and Nadia basically telling him to grow up. Poor woman is already a prisoner and now she has to deal with this giant baby too?? Now this is real torture

Oh the penthouse is at Caesar’s Palace?? Daaaamn, that’s gotta be pricey. (Also sigh,  looks like I’m gonna need to make another trip to Vegas this year to see these new locations haha). But oooohh at the meaningful eye contact between Nadia and Thony as Nadia hands her the medical file. Also he asks Thony her opinion within literally like 10 seconds of her opening the file– like give her a minute to actually read it before she gives her answer, maybe?? But oh man the tightrope she walks when she says that it could have been a drug interaction, but then follows it by saying there’s nothing in the report that indicates that that’s the case. And then ugh she immediately tries yet again to talk him into letting her and Arman handle the medication shipment. And when he tells her that the shipment has gone missing and his men are currently investigating to find out who is to blame? There’s no question for her that it was Arman, and ugh she’s trying so hard to keep her face neutral and not let the dread and anger and fear show. Because by stealing that shipment, Arman has put two of the people she loves most at risk: Luca, and himself. And even worse, she knows that in a way it’s her fault, because he did it for her. this is true love right here bitches

But ugh Nadia and Thony walking out together, and Thony’s grim expression, clearly hating that she had to tell the truth about the drug interaction because it was all a test– one that she needed to pass for the safety of her whole family– versus the fear in Nadia’s eyes and the cuttting edge to her voice as she tells Thony to tell Arman that she sold them both out?? And then the total tone change as she graciously thanks her for coming? Damn the relationship between these two is so engrossing, especially because as much as they are at odds, they do often have a lot of empathy towards one another and help each other out even when you might not expect them to. S3 please give me all the Thony and Nadia team ups please

Ooooh Garrett that was actually pretty smooth? Lucky no one was in the toilets though lol. Fair enough for him to be pretty pissed with her– she lied to him about Maya, and now she is being driven around by RK’s guys? It doesn’t look great. And aaaahh I have been waiting for this confrontation scene since the moment Maya died,  and tbh Oliver is doing a great job with expressing the hurt and anger and betrayal. And man the way Thony’s voice is so small as she tells him she’s sorry? And his “Or have you gotten so good at lying and covering up the truth that you don’t even recognise it?” like oooohhhh what a blow, and what an insightful statement. Honestly Thony needs someone to call her out like this, to make her see the path she is headed down and the ways that she has already changed. Not that I don’t want her to continue on this path haha, because getting to watch Mob Boss Thony is definitely the absolute dream (heck yeah bring on S3), but I want her to be a badass boss without losing her humanity. But tbh I love the fact that the moment she gets the call that Luca is at the hospital, it’s like the fight is immediately put on hold because it’s just understood that Luca comes before anything else.

Seriously though, Fi took him to a public hospital???? The woman who tried to stop Thony from doing the same thing in 1x02 because she was so scared she’d be deported??? Like if there was no other option, sure, but Fi literally has Dr Saroyan’s number (Thony gave it to her when she went to The Philippines) and she knows that Luca has been taken to Dr Saroyan’s clinic before? Why would she not try that first????????? Like ok tbh I would have been fine with it if there was even just a quick little throwaway line like “I tried calling Dr Saroyan but his receptionist said he’s away in Boston for a week” so it covered that plot hole. But whatevs, we need the drama I guess lol. But ugh honestly Jazz makes such a good suggestion about calling JD to take Luca inside instead– like even if he will take a little bit to get there, he could switch out with Fi so she’s not at any more risk than she needs to be? Ugh this is so dumb I don't need this stress in my life

“My nephew has a high fever and he started throwing up about an hour ago”  wait are you kidding me????  that’s all you’re going to say, Fi??? That makes it sound like simple gastroenteritis. You gotta lead with the fact that this is an immunocompromised child like 2 months post liver transplant?? Oh my god. Tbh I hate this scene for multiple reasons, partly because of the above, but also partly because of how uncomfortable it feels with the guards staring at her (though that's obviously the point), and also because it’s just a reminder of how terrible the US healthcare system is (which lbr is probably also the point). But ugh even this really lovely Filipina nurse is making me afraid that it’s all actually a trap and ICE is already on their way ughhhh I hate this

“I’m not hungry!” yep RK is definitely a child lol. But oh shit the backstory about his dad dying from a heart attack at 45 and then RK taking every possible precaution to avoid the same– like hell okay maybe he actually did get himself an angiogram and all the other fancy cardiac testing?? lol. In which case Nadia is really in trouble haha. When he had Joseph pour her the champagne (the same one she poisoned him with, naturally) I was so terrified for her ugh. Ngl I was unhappy about her throwing suspicion onto Thony about the shipment, but I mean it was pretty understandable— especially bc she felt that Thony had betrayed her first, and also tbh there was no other possible scapegoat for it except for herself or Arman. But ugh her shiny eyes as RK walks away, knowing that she is walking such a knife’s edge with him and that he might snap at any moment? Ugh my girl. Plus honestly I’d definitely like to think that she also felt at least a little bad about the fact that she may have just gotten Thony killed–  if circumstances were different, I honestly think these women could actually have been something almost like friends ugh

Ugh okay now Thony has arrived at the ER and finally someone is being made aware of Luca’s history and the urgency of the situation!!  Also damn she’s impressively persuasive given she manages to get that lady to call a code… this is making me want to fish out my old hospital ID to see whether we had a code white lol. It definitely didn't mean ‘medical emergency’ though, because naturally that one I did know, having responded to them often enough lol

Also lol I just noticed that there’s a pamphlet saying ‘stem cell therapy saves lives’ on it at the desk, and it has the initials/logo of the Institute of Stem Cell Medicine (the place where she took Luca in early S1) on it!! Like it’s probable that they were just recycling medical props from last season but I love this little easter egg omg

Ugghhhh I am still so uncomfortable about these guys being at this hospital at all. Like I get that it’s for plot reasons, creating the whole ‘what if we get noticed and deported’ tension, but it’s just so frustrating that everyone has forgotten about Dr Saroyan!! Like c'mon guys. Plus I just miss him lol, he was so softspoken and pretty. Though tbh this Dr Gonzalez is quite pretty too. In fact, pretty much every doctor that has appeared in this show has been rather attractive– seriously where were all these beautiful people during my training??? at acting school obviously lol

OOOH. Thony just said that Luca is 10 weeks post-transplant! Excellent, I’ve been meaning to put together a timeline of the TCL events, considering that the entire show literally happens over the course of like 4 months. So Luca was a week postop when he and Thony came back from Mexico (1x09) and then Marco kidnapped him like another week later (end of 1x10/start of 2x01), so looks like S2 has happened over the course of about 8 weeks. Which tbh actually seems a little long to be accurate, given that several of the eps happen literally the day after the previous ep’s events, but it could potentially work. Guess I’ll find out when I actually put the timeline together lol

Anyway is it weird that I felt proud when Dr Gonzalez said that (from the scans, I assume) Luca’s graft looks extremely clean and that a surgical complication definitely wasn’t the cause for his current condition? Like ugh damn straight my girl Thony did an incredible job on the surgery. And what a relief it must be for her to hear that she didn’t cause this, because you know that's been her greatest fear ever since she realised she was going to have to do the surgery in the first place

Stepping into the chapel to call her married(ish?) criminal boyfriend? I love it. Blaspheme away, girl, I support you wholeheartedly. I also love that she knows he was the one who took the shipment, knows he did this for her, to prove to her he meant it when he said he wouldn’t let his plan to kill Kamdar endanger Luca. But of course now that plan (along with Thony’s thwarting of it) has endangered all of them lol. Oops. Also dude I had been wondering why this ep hadn’t quite been doing it for me thus far (like of course I’m enjoying it, but just not as much as other eps) and I mean part of it is definitely the focus on Robert and also the borderline insanity of bringing Luca to this hospital, but mostly it’s because I’ve been like EXCUSE ME. WHERE IS MY BOY. WHERE IS MY PRECIOUS MURDER CUPCAKE. WHERE. Like seriously up until this point we have gotten a total of like 20 seconds of Arman onscreen and that is simply not enough for me to survive on lol. But ugh finally we are getting some good fucking food, as Gordon Ramsay would say, bc fuck yes to this entire phone exchange– Arman clearly angry and upset that she didn’t trust him enough to follow his plan (you just know he’s thinking back to their plan in 1x10 and how she trusted him then, but has since seemingly turned her back on him; dw so much more will be said on that in the next recap lol), then there’s Thony acknowledging that she made a mistake/that her choice endangered them all (aka maybe that she doesn’t always know better than everyone), and then there’s the way that all the fire immediately goes out of Arman the moment he hears how sick Luca has gotten. Ngl even though the ‘my son is dying!’ thing is getting a liiiiittle bit stale (I mean to be fair though, it is realistic for how a parent with a dying/chronically ill child would be), I do love that the two powerful men in Thony’s life will immediately put aside their own frustrations and agendas for Luca. (and, of course, for Thony herself)

“We’ll get those meds, but after that we’re done.” Honestly, I love this line, because you just know it’s not true; literally the emptiest threat my boy has ever made haha. But it’s important for it to be said anyway– considering that Arman has already established to Thony through both words and actions that he will do pretty much anything for her, the act of telling her that they’re done is one of the only ways he can express to her how much she has hurt him without literally saying those exact words aloud. (It’s probably also partly habit from his fights with Nadia, too; I don't doubt they've both threatened each other with divorce multiple times lol, which is extra funny now we know they were never married in the first place).  But anyway lbr here, he’s never going to follow through on this threat with Thony, just like he didn’t in 2x05 after he said it the first time. But the point is that there’s still just enough uncertainty there– the possibility that maybe this time he really does mean it– that it kinda forces Thony to examine her choices and face the idea that unless she trusts him and lets him be her equal partner in this, she might lose him. But ugghhh at him immediately grabbing all the money he has left in the world and coming out of hiding to help her save Luca. Just like she knew he would, before he even answered the phone– because like she told Fi: he always shows up when she needs him. 

Also, catch me screaming over the fact that the man has no reason to have her motorbike helmet with him, but does anyway??? Like last we saw him, he was at La Habana on the phone with Nadia, finding out about Kamdar, and presumably he went right home and got the essentials to take into hiding– which apparently includes Thony’s motorbike helmet. Y’know, just in case she called, needing him. I’m so fine and normal about this I swear

Actually you know what, I'm not fine at all, because we were absolutely robbed of the scene where she manages to sneak out the back of the hospital and he pulls up to get her and just silently holds out the helmet, and then on the ride it really hits her that maybe he will  walk away after all this and that it will be all her fault, and between that terrible feeling of dread and her overwhelming fear for Luca she starts to cry silently, her arms clinging to him tighter than usual because she’s so terrified she’s about to lose two of the people she loves most, and then at one point they’re stopped at a traffic light and he covers one of her hands with his and squeezes, like he can sense that she’s barely keeping herself together, and she cries harder because if she still has him then maybe it will all be okay, maybe they will get the meds and get back to Luca in time and maybe she can stop trying to carry all this weight on her own and–

But anyhow, I digress lol. I love that Arman steps straight into the office and barely spares the guy a glance as he grabs the bolt cutters and the paper with the container number on it. Man is on a mission to save his future stepson lol, and god help anyone who gets in his way. And ugh I just love everything about his and Thony’s teamwork– she finds the container and he comes running with the bolt cutters; he starts cutting the inventory lists free and handing them off to her, letting her guide him to the right spot. They just work so naturally together without needing to discuss it and idk man I am just very into everything they do together lol (and boy i would sure love for them to do some ~other~ stuff together lol)

God the look of terror on her face when they hear the cars screech into the shipping yard, and the way he whispers a reassurance to her and touches her arm for just a second as he passes? And then he peeks around the corner and sees several of Kamdar’s men being pointed their way (damn that little rat bastard for selling them out) and ugh I want to hug him because he knows how bad these odds are, knows that he might be about to die right now but that doesn’t matter, all that matters is keeping them from getting to Thony. Like ughhhhhh “I’ll do what I can to hold them off” and then him locking her inside the container?? He knows she has her phone, knows that even if he dies taking all the men out then she will still be able to call for help, so he takes every measure he can to keep her safe and give her the best chance of survival. I also stupidly love that it’s his knife that she’s using to cut out and search the inventory lists, and his knife that is her only weapon/defense. Just another way he protects her ugh

Though lol at him choking the guy out in like 5 seconds while the guy doesn’t even fight it. Kamdar would be embarrassed to be associated with such a pathetic goon lol. Ngl tho I very much enjoy watching Arman getting beaten up and thrown into objects and still getting up and keeping fighting because this is a fight he simply cannot afford to lose ugh

Okay these writers definitely do not know how to write delirious kids lol, but I forgive them. However I don’t forgive the nurse guy who Fi goes to for help, considering he glances at the monitor for half a second and then says Luca is probably just tired. Like seriously how did this guy get through nursing school? And then lol the next minute Luca has a tiny bit of a nosebleed (not even actively dripping) and Dr Gonzalez gets someone running in with a procedure cart to shove unnecessary packing up his nose. Like hey guys can you maybe try to find a happy medium between under- and overreacting lol??

God Thony dropping the phone and not being able to reach it makes me feel so stressed, and then ugh her being found because Fi keeps calling her??? Reminds me of 1x01 and Fi’s call being the reason she gets found and thrown in front of Arman in the first place. The woman really needs to learn to put her ringer on silent lol. But god how badass that she literally climbs her way out and runs across the top of the container and makes a jump for it? Like damn Arman was right, she really has learned a few things lol. Also fucking love Arman seeing Thony getting cornered by two gunmen and responding by immediately taking out his own guy (by fighting dirty, throwing sand in his eyes and then kicking him in the balls, to which I say hell yeah) before diving for his gun and shooting the guy who was about to shoot Thony. And then taking out the other guy too, before yelling for her to get down and killing the guy who had just appeared out of the container behind her (what that guy was still doing in the container for so long when Thony had already escaped, who knows lol). And ugh when he signals for her to run over to him, she doesn’t hesitate, just knows that he will cover her and make sure she makes it safely, and then they make their escape together on the bike with him shooting the last two guys while racing out of there??? Like honestly this man needs to go straight back to jail because being this sexy is a goddamn CRIME

Ugh, yet again we were robbed of the possible Armony though– like excuse me, where is my scene of her clinging to him again as he races them back to the hospital, then the two of them frantically asking each other if they’re okay/uninjured before he reassures her he’s fine and sends her back in to save Luca, telling her to call him as soon as she has news?? Like seriously where is it, writers??? I need ALL the Armony ugh

Ngl I’m on Dr Gonzalez’s side here lol, bc what Thony is proposing to do is legit crazy– not to mention both illegal and unethical, which would be sOO MUCH LESS OF A PROBLEM IF Y’ALL HAD GONE TO MY BOY DR SAROYAN INSTEAD, BUT NOOOOOOOO. Like again, I know that they had to end up at a proper hospital for the plot, but ugh that doesn’t stop the plot from being annoying lol. Though tbh I do love that they can only achieve their plan of sneakily giving Luca the treatment he needs because of their little network of cleaning ladies haha. Who run the world???? 

Lbr tho this girl is taking a huge risk for them– I appreciate the writers at least giving the explanation that it’s in thanks for Thony delivering Nina’s baby, but still, can we at least try to minimise her involvement so she doesn’t go down with you??? In fact, get Fi the hell out of here too, you don’t need her! Especially since Luca apparently needs to be ventilated for 36 hours for the drug to work, which means it is literally impossible for them to NOT get caught doing this. Aaaaahhhh I am so stressed lol. Aaand yep they’ve been caught by Dr Gonzalez already, who actually kind of seems like he might go along with it– what is it about the Thony & Luca combo that men just can’t say no to lol?? lbr I would not say no either sooo

Like lol Garrett literally admits it to Russo, that he was right in the middle of yelling at Thony and then let her go the moment there was a call about Luca. He really does get too close to his CIs and tbh I love that about him because it’s both a flaw and one of his main redeeming attributes. And ugh when he tells her that he believed Arman when he said that it came down to a choice between Thony or Maya (love the fact that both Russo and Garrett are well aware just how much Thony means to Arman), and that Arman is a criminal who actually tells the truth? Which is ironic because Garrett is a law enforcement officer that will lie and manipulate people all day long if it serves his purpose. Like yesss this is what the show has been saying all along– people aren’t just black and white, good and bad. The world is complicated and grey and what’s ‘right’ isn’t always clear

Speaking of complicated though, oh god Garrett and Russo. What are you two doing. Like I appreciate that Garrett says he’s a mess and needs to figure himself out, that was very mature of him…… aaaaaand now they’re hooking up lol. I still can’t get over the fact that timeline-wise, it’s been like a week since Maya’s death, but hey I guess everyone copes in their own way or whatever lol

Uggghhhh god it is so hard to watch this scene with Dr Gonzalez bringing in the cops and child services, but tbh are you REALLY so shocked, Thony?? Honestly she has been just getting away with shit for far too long, and even when there’s repercussions (like Arman or Garrett getting pissed with her) she gets forgiven quickly enough that it seems she’s forgotten that she might actually have to face real, permanent consequences. (Again, Marco who?? lol) But I do kinda love how angry and disbelieving she is about them taking her away, because it is so fitting for her character, and fits with the way she deals with fear/panic. But again I’m just saying Thony, you could have been sipping coffee with Arman at Luca’s bedside in Dr Saroyan’s clinic rn, but instead Luca is being taken from you, and you and Fi are in handcuffs. Sigh why do these fictional characters never listen to me

Omg wtf RK is trying to drown Nadia?????? No fucking way will I allow this. Ok that’s it, I’ve been saying all along that this dude gotta die and now there’s no going back. KILL HIM NADIA. MAKE HIM REGRET BEING BORN

[whumpster-dumpster]

how can someone rupture their bladder, and how long can they go without medical attention?

Most of the time it’s caused by blunt force trauma and pelvic fractures associated with car and motorcycle accidents. Sometimes it can also be caused by a long fall, something heavy falling on the abdomen, gynecological and colorectal surgery, urologic procedures, and Foley catheter placement.

I couldn’t find an exact time for how long you can survive but if untreated, it can lead to severe complications such as sepsis, renal failure and hyperkalaemia, and can eventually cause death.

[cat-brodsky]

Poisonous flowers to grow in your garden: Foxglove

DISCLAIMER: This post is for educational purposes only. You assume moral and legal responsibility if anyone gets hurt by a plant that you grow. Make sure that your garden is not accessible by anyone who is ignorant of the danger, especially children or animals.

Foxglove (Digitalis) is a genus of about twenty biennial (lives for two years) and perennial (lives for more than two years) herbaceous plants and shrubs. Common foxglove (Digitalis purpurea) is the most common garden variety, with many cultivars to consider.

They can grow rather tall - up to two metres (six feet) for the common foxglove. The leaves are oval, hairy, with a toothed margin; they start out in a rosette, with alternating distribution on the stem.

The flowering season is in early summer (late spring in warmer zones). The flowers themselves are dainty, beautiful, and deadly. They’re arranged in an elongated cluster, with each flower large enough to fit over a finger like a thimble (as you can guess by the name). They’re usually purple in colour, with the inside heavily spotted, but white, pink, or yellow cultivars also exist.

Peloric mutations, where a plant produces a flower with an abnormal number of petals and radial, star-like symmetry, are also very common in foxgloves.

A peloric D.purpurea flower.

Favoured conditions

Temperature range: Seeds germinate at soil temperature above 20C (70F). Foxgloves are hardy at zones 4-10 (look your region up on the hardiness zone map), but may wilt if it gets hotter than 30C (90F)

Light: From full sun to partial shade. Foxgloves are woodland flowers, so they can tolerate lack of sunlight.

Soil: Any texture (sand, clay, or silt), with rich (fertile) soil preferred. Some sources say they prefer acidic soil, others say neutral pH. Both are certainly acceptable.

Water: Keep the ground moist but not wet; soil needs to be well-draining. No air humidity requirements.

Growing tips

Foxgloves propagate by seed. Like any biennial, foxgloves flower in their second year, so be patient and make sure to plant seeds for two years in a row to make sure you get flower annually.

They’ll self-sustain if allowed to re-seed themself, so you can leave the plants alone. But you can also remove wilted flowers - this is called deadheading and promotes a second bloom - or you can harvest the seeds yourself.

After the first year, cut the plant down to the crown, and cover in mulch if living in a colder region. If the flower clusters get too large, or if there is harsh weather such as wind or hail, they may require staking.

Foxgloves can be grown in containers, just make sure to pick one that’s sufficiently big. All in all, this is a plant that doesn’t require much fussing over.

Toxicity

That’s what you’re here for, aren’t you? All right.

Digitalis species contain a number of cardiac glycosides, specifically, cardenolides. Digoxin and digitoxin are the most studied of those.

Pharmacology:

Cardenolides are toxic to mammals through inhibition of Na+/K+‐ATPase, also known as the sodium-potassium pump. The differing concentrations of ions outside and inside a cell are used to maintain resting potential (to put it in an overly simple way: difference in charge on the inside and the outside), which, in excitable cells such as cardiac muscle or nerve cells, is crucial to their proper functioning.

Digoxin interferes with the functioning of the Na⁺/K⁺ pump; this results in an increased Na⁺ concentration inside the cell. That, in turn, leads to an increase in Ca⁺⁺ ions (because of another ion pump). Ca⁺⁺ influences heart contractions: heart rate goes down, blood pressure goes up, stroke volume increases.

As you might imagine, there’s a number of things that can go wrong. Bradycardia (low heart rate) or arrhythmia can ensue, which can lead to a cardiac arrest. Hyperkalaemia (high K+ concentration) can induce arrhythmia, but so can hypokalaemia (low K+ concentration) - more K+-binding sites are open for digoxin, increasing the effective concentration of digoxin within the heart.

Every part of the plant is highly toxic. Symptoms are non-specific: nausea, vomiting, abdominal pain, headache, increased respiration rate, excitation, drowsiness, dizziness, apathy, confusion, and delirium. Vision disturbances can also happen - a specific interesting symptom is xanthopsia, seeing the world tinted with yellow. And, of course, cardiac disturbances - irregular heartbeat, ventricular tachycardia, ventricular fibrillation, sinoatrial block and AV block. In short, the most likely cause of death from a foxglove poisoning is cardiac arrest following arrhythmia or V-fib.

Detection: Very trivial. Elevated K+ levels and a particular appearance of the EKG - both would lead to a blood test being conducted, which should reveal the presence of digoxin.

Happy Halloween.

This was going to be a post on several different plants, but foxglove alone proved far too long. I’m breaking it into a series, so watch this space for more.

[doctorfoxtor]

post ain't long it's wrong, can't study till dawn? yawn

100 days of productivity

day 44 + 45

CVS/RS

rheumatoid pleural effusions closely mimic complicated parapneumonic effusion on analysis, w/ ph <7.2, marked ↑LDH and notably glucose <30 (in fact glucose >30 almost rules out rheumatoid effusion)

in afib, digoxin will slow ventricular rate but is unlikely to cardiovert the rhythm

itraconazole in ABPA causes a 50% reduction in steroid dose and 25% reduction in anti-aspergillus IgE, and either partial or complete resolution of CXR infiltrates or improvement in PFTs/exercise tolerance

TRALI can happen as early as 15 minutes into the transfusion apparently?????

mesothelioma is an abject death sentence. The most you can do for patients beyond stage 1 is chemotherapy (limited survival benefit with platinics), radiotherapy to biopsy/thoracoscopy tracts only and surgery (lung-sparing debulking ± pleurodesis for recurrent effusions; radical surgery has shown no survival benefit)

mild tachy + broad qRs in haemodynamically stable pt s/p PCI for MI → likely to be LBBB developing; watch and wait

CNS/Ophthal/Psych

PSP looks similar to parkinson's bc it affects the opposite pathway as parkinsons (striatonigral vs nigrostriatal)

the best response you can get from deep brain stimulation for parkinsons = the best response you got from medication; DBS will NOT add a greater response compared to maximum medical therapy

without any other information, parkinson's ssx w/ dementia WITHIN 1 year of onset, it's Lewy body dementia; if it's more than 1 year, it's parkinson's w/ 2° dementia

choroidal neovascularisation with NO OTHER fundal signs: wet mac degen > diabetic retinopathy

focal dystonias are better treated with botox than with medication

SAH is unlikely to cause cranial nerve palsies other than III and maybe VI; pituitary apoplexy presents similarly with very severe headache/projectile vomiting/AMS, while affecting nerves III, IV, V-1 and VI

MS relapse: 500 mg PO or 1 g IV methylpred x5 days

there is no difference in risk of progression to Korsakoff when Wernicke is treated w/ glucose first vs w/ thiamine first

Endocrine/Repro

hyperaldosteronism: hyperplasia > adenoma

acute alcohol consumption can trigger hypoglycaemic events as the liver uses up NAD+ for each step of the alcohol detox pathway, where NAD+ is an important cofactor for the malate-oxalate shuttle used in gluconeogenesis

cinacalcet's major indication is hyperparathyroidism taht can't be corrected w/ surgery (eg, unfit pts)

Rheum/Derm/Immuno

topical steroid potency: hydrocortisone < clobetasol butyrate, betamethasone valerate low-dose < betamethasone valerate high-dose, fluticasone propionate < clobetasol propionate

onycholysis: trauma, tinea (infections), thyrotoxicosis, tetracyclines

pseudoxanthoma elasticum is assoc w/ mitral prolapse, renovascular htn, PVD, CAD, GIT bleeds and retinal vessel abnormalities

IgE values are normally distributed, so about 2.5% of the pop has raised IgE and 2.5% has reduced

s/p parathyroidectomy → acute drop in PTH → bones that are used to high levels of PTH experience a relative hypoPTHism → ↑blastic ↓clastic activity → acute bony uptake of calcium, PO4 and importantly magnesium = hungry bone syndrome (replace calcium and magnesium!)

carpal tunnel pain can radiate retrogradely to the forearm and sometimes even the arm

periarticular osteoporosis → RA

punched out erosions in juxtaarticular bone → gout

GIT

Peutz-Jeghers: small bowel hamartomas → intussusception, colorectal cancer, pigmented lesions (classically perioral/mucosal, but also palms/soles)

pernicious anaemia: parietal cell Abs (common) > intrinsic factor Abs (specific)

haemochromatosis: venesection → keep ferritin <50 and transferrin sat <50%

passing stools frequently, elevated inflammatory markers, ↑faecal calprotectin, PPI but not in demographic for IBD → take a colonoscopy and biopsy, this is probably microscopic colitis (and PPIs can trigger at any age)

liver biopsy is not indicated for Gilbert's—it is sufficient to do routine CBCs/LFTs w/ bilirubin analysis

pancreolauryl (fluorescein dilaurate) is quite nonspecific and will not pinpoint the exact pancreatic disease

hep A can be precided by short diarrhoeal illness`

in an IBD (esp UC) pt who comes >10 yrs after initial symptoms with recent change in bowel habits, offer urgent colonoscopy to r/o ca colon BEFORE starting on treatment

Onc/Haem

MTX + antifolate antibiotics: makes sense not to give them together—they can cause fulminant marrow failure

leukaemia can very rarely lead to acute painful scrotal swelling

5q- syndrome = myelodysplasia, but with thrombocytosis; diff from essential thrombocythaemia by anaemia with normal reticulocyte count and leukopaenia in the former

radiotherapy is a primary modality of tx in retinal, CNS, skin, oesophageal, cervical, vaginal and prostatic tumours; it is adjuvant in all other tumours

the commonest presentations of CMV s/p txp are pneumonia or pulmonary infiltrates

Renal/Biochem

SIADH causing drugs - SIADH Causes Poor Voiding: Sedatives (barbiturates), Indomethacin (NSAIDs), Antidepressants (TCAs/SSRIs), thiazide Diuretics, 1st gen antiHistamines, Cyclophosphamide/antiConvulsants, 1st gen antiPsychotics, Vinca alkaloids

malaria: irreversible nephrosis (esp memb or FSGS) > nephritis

2° syphilis: reversible nephritis > nephrosis

even if the patient doesn't qualify for ACEis/ARBs for HTN, give them first-line anyway if concomitant renal disease

kidney size difference >1 cm is significant

for drugs that will be dialysed out on dialysis days, dose them immediately after dialysis on those days

only urge incontinence is not primarily managed with pelvic floor exercises

Pharm/Toxo

valproate ADRs - VALPROATE: Vomiting, Alopecia/Anorexia, Liver tox, Pancreatitis/PCOS, Redistributed fat (weight gain/lipodystrophy), Oedema, hyperAmmonaemia/Ataxia, Tremor/Thrombocytopaenia, Enzyme inhibitor

opioid withdrawal: methadone is the best single tx and avoids needing to give multiple drugs to cover ssx (eg, clonidine + dextromethorphan + loperamide)

aminoglycosides preferentially affect proximal tubular cells

the classic pattern of symptoms in both cotton workers and workers at factories that process nitrates is that of 'Monday disease'

toxicities for which measuring the blood levels is indicated - SLIME TiPP: Salicylates, Lithium, Iron, Methanol, Ethylene glycol, Theophylline, Paraquat, Paracetamol

amphetamine tox → hyponatraemia due to water retention, worsened by the excessive thirst; hyperkalaemia → rhabdo; hypokalaemia not seen because amphetamines tho sympathetomimetic do not have affinity for the β2 receptor like cocaine does

[biomedicool]

Kidney function tests

Creatinine

Creatinine is a waste product produced in muscles from the breakdown of a creatine. 

Creatine is part of the cycle that produces energy needed to contract  muscles. 

Both creatine and creatinine are produced at a relatively constant rate. 

Almost all creatinine is excreted by the kidneys, so blood levels are a good measure of how well your kidneys are working.

If low: 

Low levels are not common and are not usually a cause for concern. 

As creatinine levels are related to the amount of muscle the person has, low levels may be a consequence of decreased muscle mass (such as in the elderly) but may also be occasionally found in advanced liver disease.

If high:  

Kidneys break down creatinine - if levels are high, they’re not working properly -->

Damage to or swelling of blood vessels in the kidneys (glomerulonephritis) caused by, eg, infection or autoimmune diseases bacterial infection of the kidneys (pyelonephritis)

Death of cells in the kidneys’ small tubes (acute tubular necrosis) caused, for example, by drugs or toxins

Prostate disease, kidney stone, or other causes of urinary tract obstruction.

Reduced blood flow to the kidney due to shock, dehydration, congestive heart failure, atherosclerosis, or complications of diabetes

Creatinine blood levels can also increase temporarily as a result of muscle injury and are generally slightly lower during pregnancy.

Urea

Urea is the final breakdown product of the amino acids found in proteins. Nitrogen in the form of ammonia is produced in the liver when protein is broken down. The nitrogen combines with other chemicals in the liver to form the waste product urea.  Healthy kidneys remove more than 90% of the urea the body produces.

If Low: 

Low urea levels are not common and are not usually a cause for concern. They can be seen in severe liver disease or malnutrition but are not used to diagnose or monitor these conditions. Low urea levels are also seen in normal pregnancy.

·   If high: 

High urea levels suggest poor kidney function. 

Acute or chronic kidney disease. 

However, there are many things besides kidney disease that can affect urea levels such as decreased blood flow to the kidneys as in congestive heart failure, shock, stress, recent heart attack or severe burns; bleeding from the gastrointestinal tract; conditions that cause obstruction of urine flow; or dehydration.

Albumin

Albumin is the most abundant protein in the blood. It keeps fluid from leaking out of blood vessels; nourishes tissues; and transports hormones, vitamins, drugs, enzymes, and ions like calcium throughout the body. Albumin is made in the liver and is extremely sensitive to liver damage. 

If low:

Low albumin concentrations in the blood can suggest liver disease. Liver enzyme tests are requested to help determine which type of liver disease.

Diseases in which the kidneys cannot prevent albumin from leaking from the blood into the urine and being lost.

Also seen in severe inflammation or shock.

Conditions in which the body does not properly absorb and digest protein such as Crohn’s disease.

If high: 

High albumin concentrations in the blood usually reflect dehydration.

This is a very long list so click keep reading to read the rest!

Phosphate

In the body, phosphorus is combined with oxygen to form a variety of phosphates (PO4). Phosphates are vital for energy production, muscle and nerve function, and bone growth. They also play an important role as a buffer, helping to maintain the body’s acid-base balance.

If low:  (hypophosphataemia)

Hypercalcaemia (high levels of calcium), especially when due to high levels of parathyroid hormone (PTH)

Overuse of diuretics (drugs that encourage urination)

Severe burns

Diabetic ketoacidosis after treatment

Hypothyroidism

Hypokalaemia (low levels of potassium)

Chronic antacid use

Rickets and osteomalacia (due to Vitamin D deficiencies)

Increased production of insulin

If high:  (hyperphosphataemia) 

 Kidney failure

 Hypoparathyroidism (underactive parathyroid gland)

 Hypocalcaemia (abnormally low levels of calcium)

 Diabetic ketoacidosis when first seen

 Phosphate supplementation

Alkaline phosphatase

Alkaline phosphatase is an enzyme found in high levels in bone and liver. Smaller amounts of ALP are found in the placenta and in the intestines. Each of these makes different forms of ALP (isoenzymes).

If low

Zinc deficiency. Magnesium deficiency. Anaemia. Poor nutrition.

Hypophosphatasia (Metabolism disorder, in born). Hypothyroidism.  Wilsons disease. 

If High: 

Raised levels of ALP are usually due to a disorder of either the bone or liver. 

If other liver function tests are also raised, this usually indicates that the ALP is coming from the liver. 

However, if calcium and phosphate measurements are abnormal, this suggests that the ALP might be coming from bone.

In some forms of liver disease, such as hepatitis, ALP is usually much less elevated than AST or ALT. 

However, when the bile ducts are blocked (for example by gallstones, scars from previous gallstones or surgery, or by a tumour), ALP and bilirubin may be increased much more than either AST or ALT. 

ALP can also be raised in bone diseases such as Paget’s disease (where bones become enlarged and deformed), in certain cancers that spread to bone or in vitamin D deficiency.

Calcium

 99% of calcium is found in the bones, and most of the rest circulates in the blood. Roughly half of calcium is referred to as 'free' (or 'ionized') and is active within the body; the remaining half, referred to as 'bound' calcium, is attached to protein and other compounds and is inactive.

If low: (hypocalcaemia)

The most common cause of low total calcium is low protein levels, especially low albumin. When low protein is the problem, the 'free' calcium level remains normal. 

Underactive parathyroid gland (hypoparathyroidism)

Decreased dietary intake of calcium

Decreased levels of vitamin D

magnesium deficiency

too much phosphate

acute inflammation of the pancreas

chronic kidney disease

calcium ions becoming bound to protein (alkalosis)

bone disease

malnutrition, and alcoholism.

 If high: (hypercalcaemia)

Hyperparathyroidism (increase in parathyroid gland function) usually caused by a benign tumour on the parathyroid gland. 

Cancer when spread to the bones, which releases calcium into the blood, or when it causes a hormone similar to PTH to increase calcium levels.

Hyperthyroidism, Sarcoidosis, Tuberculosis, Too much Vit D, Drugs that increase diuretics.

Potassium: 

Abnormal concentration can alter the function of the nerves and muscles.

If low: (hypokalaemia)

vomiting,

diarrhoea, and insufficient potassium intake (rare).

In diabetes, potassium concentration may fall after insulin injection.

If high:

(hyperkalaemia)

kidney disease

Addison's disease

tissue injury

infection

diabetes

excessive intravenous potassium intake (in patients on a drip)

Glucose: 

If low: (hypoglycaemia)  

Adrenal disease (Addison's disease)

Alcohol/ drugs, such as: paracetamol and anabolic steroids

Extensive liver disease

Hypopituitarism

Hypothyroidism

Insulin overdose

Insulinomas (insulin-producing pancreatic tumours)

If high: 

High levels of glucose most frequently indicate diabetes, in fasting blood glucose test: <7mmol/L is indicative and in oral glucose test ites <11 mmol/L .

Acromegaly

Acute stress (response to trauma, heart attack, and stroke for instance)

Long-term kidney disease

Cushing's syndrome

Drugs, including: corticosteroids, tricyclic antidepressants, oestrogens (birth control pills and hormone replacement therapy [HRT]), lithium..

Hyperthyroidism

Pancreatic cancer. Pancreatitis

Triglyceride: 

Most triglycerides are found in fat (adipose) tissue, but some circulate in the blood to provide fuel for muscles to work. 

If low: 

Hyperthyroidism. Malnutrition. Certain medications and drugs can deplete fat, leading to low triglycerides. 

If high: (e.g. at least 10-15 mmol/L) --> pancreatitis. 

Parathyroid hormone: 

Part of a ‘feedback loop’ that includes calcium, PTH, vitamin D, and to some extent phosphate and magnesium.  PTH is secreted into the bloodstream in response to low blood calcium concentration. 

If both PTH and calcium results are normal, and appropriate relative to each other, then it is likely that the body’s calcium regulation system is functioning properly.

Low --> conditions causing hypercalcaemia, or to an abnormality in PTH production causing hypoparathyroidism. 

High --> hyperparathyroidism, which is most frequently caused by a benign parathyroid tumour.

Calcium - PTH Relationship

Calcium  low and PTH high, then PTH working. Low calcium may be investigated.

Calcium  low and PTH normal or low --> hypoparathyroidism.

Calcium high and PTH  --> hyperparathyroidism.

Calcium  normal and PTH high --> vitamin D deficiency or chronic kidney disease.

Amylase

Released from the pancreas into the digestive tract to help digest starch. It is usually present in the blood in small quantities. When cells in the pancreas are injured or if the pancreatic duct is blocked (by a gallstone or rarely by a tumour) increased amounts of amylase find their way into the bloodstream.

If high:

 Pancreatitis which is a severe inflammation (often 5-10 times normal)

Cancer of the pancreas, gallbladder disease, a perforated ulcer, obstruction of the intestinal tract, mumps or ectopic pregnancy. 

Increased blood amylase with normal or low urine amylase may indicate decreased kidney function or the presence of macroamylase.

[biology-geology-beaches-india]

TSRNOSS, page 175.

[palvichemical]

Medical Applications, Importance & Adverse Effects of Sorbitol

Sorbitol is a sugar alcohol or polyol, which are water-soluble molecules found naturally in many fruits and vegetables. Sorbitol is also commercially synthesised from glucose for usage as a sweetener, texture, and moisture retainer in packaged foods and beverages.

Medical Applications:

●   Laxative:

Sorbitol-containing meals, like other sugar alcohols, can cause gastrointestinal irritation. Sorbitol can be used as a laxative either orally or through an enema. Sorbitol acts as a laxative by attracting water to the large intestine and promoting bowel motions. Sorbitol has been found to be safe for elderly people to take, yet it is not recommended without the guidance of a doctor. Sorbitol is found in various dried fruits and may contribute to prunes' laxative properties. In 1872, sorbitol was identified in the fresh juice of mountain ash berries.

 Palvi Chemicals is the distinguished Sorbitol exporter in Nigeria.

●   Other medical applications:

Sorbitol is used in bacterial culture media to differentiate pathogenic Escherichia coli O157:H7 from most other E. coli strains because it is unable to ferment sorbitol, unlike 93 percent of known E. coli strains.

 Sorbitol and the ion-exchange resin sodium polystyrene sulfonate are used to treat hyperkalaemia (high blood potassium) (tradename Kayexalate). In the bowel, the resin exchanges sodium ions for potassium ions, while sorbitol aids in elimination. The Food and Drug Administration of the United States issued a warning about the increased risk of gastrointestinal necrosis with this combination in 2010.

 Sorbitol is also utilised in the production of softgel capsules, which are used to store single doses of liquid medications.

 Palvi Chemicals is one of the most popular Sorbitol suppliers in Ghana.

Medical importance:

Aldose reductase is the first enzyme in the sorbitol-aldose reductase pathway, and it is responsible for converting glucose to sorbitol as well as galactose to galactitol. Long-term hyperglycemia with poorly controlled diabetes frequently results in too much sorbitol trapped in retinal cells, lens cells, and Schwann cells that myelinate peripheral nerves. This can harm these cells, resulting in retinopathy, cataracts, and peripheral neuropathy. Aldose reductase inhibitors, which are drugs that impede or decrease the action of aldose reductase, are now being studied as a means of preventing or delaying severe consequences.

 If you are looking for one of the most recognized Sorbitol distributors in Ghana, Palvi Chemicals is the right place for you to fulfill all your chemical requirements.

Adverse medical effects:

As a result of small intestinal damage, people with untreated celiac disease frequently have sorbitol malabsorption. Sorbitol malabsorption is a common source of symptoms that persist in gluten-free people. Because of a strong link between the cut-off value and intestinal lesions, the sorbitol hydrogen breath test has been proposed as a diagnostic for detecting celiac disease. Nonetheless, while it may be useful for research, it is not yet suggested as a diagnostic tool in clinical practise.

Sorbitol added to sodium polystyrene sulfonate (SPS, used to treat hyperkalemia) has been linked to gastrointestinal problems such as haemorrhage, perforated colonic ulcers, ischemic colitis, and colonic necrosis, particularly in uremia patients. Immunosuppression, hypovolemia, the surgical context, hypotension after hemodialysis, and peripheral vascular disease are all risk factors for sorbitol-induced injury. As a result, SPS-sorbitol should be used with caution in the treatment of hyperkalemia.

[quilavastudy]

Hiya Hallie! Would you happen to have any tips for PSA? Would appreciate if you could share any resources that were useful for you. Thanks xx

Ok PSA post incoming, cos I’ve got a few questions about this!

First of all, try not to worry too much. This exam is different to other exams in that if you don’t know something, you can look it up. 

This is how I revised for it and I got 85%:

1. In the months leading up to the exam, just try to do a bit of revision on drugs in general - I wrote summary sheets on the most common drugs. It’s good to do this anyway for finals. I recommend the book ‘the top 100 drugs’. Things like indications, side effects, common interactions blah de blah.

2. When it gets to 1-2 months before the exam, start proper PSA-focused revision. I recommend getting the ‘pass the PSA’ textbook because that’s good for familiarising yourself with the type of questions they ask. However, bear in mind that the questions in this book are slightly easier than the real thing.

3. A few weeks before the exam, start doing the practice papers on the PSA website. These are very similar to the real thing, so do them properly, and review your answers, note the sections where you lost the most marks. I think there’s 3, I did them all twice.

Some tips:

- especially make sure you practice the calculations, because they’re not too bad but it’s easy to get in a tizz about them in the real thing. Definitely learn the main types of calculations like the back of your hand!

- practice looking things up in the online BNF. This is practically the whole exam, because unless you’ve got a photographic memory you probably will have to look up drugs for at least half the questions. Being fast on the online BNF will gain you marks. The test is quite time-pressured. Remember to use control+F to find words!

- However, I’d recommend learning some lists of drugs which cause common side effects. There’s almost always questions on drugs that cause hypo or hyperkalaemia, so learn those. Also drugs that cause confusion/drowsiness e.g. diazepam, opioids. You won’t have time to check every drug in the BNF to see if it has a certain side effect so definitely try to learn which drugs cause which common side effects! Again, the Pass the PSA book will help you with that.

- revise fluid prescribing as well, because there’s usually a big question on that

Hope that helps! x

[theoddvet]

Anaesthetic Problems and How to Fix ‘Em

Anaesthesia can be fraught with morbidity and mortality due to the sheer number of things that can go wrong in a drug-induced sleep without correct monitoring and trouble-shooting. The animal loses their ability to thermoregulate, their cardiovascular and pulmonary systems becomes depressed, and they lose many reflexes that are vital for controlling blood pressure, peripheral vascular resistance, and more.

So, let’s begin. I’ll put a read-more option because this post is fairly long.

AIRWAY OBSTRUCTION

How to recognise it --> Reduced tidal volume, chest doesn’t rise with  intermittent positive pressure ventilation (IPPV), hypoxia and hypercapnia, inadequate depth, rebreathing or flat line capnograph (partial vs total), whistling sound, apnoea

What causes it --> Intubated patients: kinked ET tube, blocked ET tube with secretions, faulty cuff, laryngospasm. Non-intubated: material blocking the pharynx, laryngospasm, anatomical defects (e.g. elongated soft palate)

How to fix it --> If intubated, suction the ET tube, extend the head and neck, give oxygen, and replace the ET tube if necessary. Otherwise, PREVENTION! Pack the pharynx for oral procedures, gentle intubation, appropriate timing of extubation, proper patient positioning 

REBREATHING (breathing in CO2)

How to recognise it --> Hypercapnia; ETCO2 >55 mmHg or inspirational CO2 >0 mmHg, brick red mucous membranes, hypertension, tachypnoea/increased tidal volume, apparent increased anaesthetic depth

What causes it --> Faulty one-way valves in rebreathing circuits, inadequate fresh gas flow in non-rebreathing circuits, increased dead space (leaks, long ET tube), or exhausted CO2 absorber.

How to fix it --> Maintain/replace equipment, ensure gas flow rates are adequate (300-500 ml/kg in a non-rebreathing circuit), minimise dead space with correct ET tube size, change CO2 absorber, supplement oxygen and IPPV,

LEAKING (of gas within the anaesthetic circuit)

How to recognise it --> failed pressure checks prior to anaesthesia (leaking >200 ml/min at 20 mmHg pressure), signs of rebreathing and hypoxia, inadequate depth control, air pollution (smell, hissing), chest not rising with IPPV

What causes it --> Faulty equipment machine or breathing circuit, ET tube cuff not adequately inflated.

How to fix it --> Maintain equipment properly, inflate cuff sufficiently (no leaking heard from trachea when reservoir bag squeezed up to 20 cm H2O)

BAROTRAUMA (pressure trauma to the lungs)

How to recognise it --> Pressure >45 cmH2O in healthy or 14-16 cm H2O in compromised patients, distended reservoir bag, apnoea or dyspnoea, tachycardia, hypotension,cyanosis, loss of lung sounds, SC emphysema, cardiac arrest

What causes it --> Prolonged closing of the pop-off valve, flushing the circuit with patient connected, IPPV with too high pressure, lung pathology 

How to fix it --> Use positive end expiratory pressure (PEEP) ventilation, oxygen, fluids and cardiovascular support, ensure the ET cuff leaks >20 cm H2O, keep pop-off valve open

TACHYCARDIA (higher than normal HR)

How to recognise it --> HR >140-160 bpm in a dog, or >180 bpm in a cat; using a stethoscope, doppler, pulse oximetry, or ECG

What causes it --> Anaesthetic plane that is too light, painful or strong stimuli, hypovolaemia, hypotension, anaemia, hypercapnia, hypoxaemia hyperthermia, heart disease, drugs such as atropine and ketamine

How to fix it --> Deepen anaesthesia, give analgesia, IV fluid therapy, oxygen and IPPV, active cooling, positive ionotropic agents such as dopamine/ dobutamine/ ephedrine for hypotension, fluids, wait for drugs to wear off

BRADYCARDIA (lower than normal HR)

How to recognise it --> HR <60 bpm in dogs, or <100 bpm in cats

What causes it --> Anaesthetic plane that is too deep, hypertension, vagal stimulus, drugs such as propofol, opioids, or alpha2-agonist sedatives, hypothermia, hyperkalaemia, increased intra-cranial pressure (ICP), decompensated hypoxaemia

How to fix it --> Lighten anaesthesia, give analgesia, warm the patient, give oxygen and IPPV, treat for increased ICP if also hypotensive with mannitol/ furosemide, fluid therapy with calcium/dextrose +/- insulin for hyperkalaemia, atropine if not hypothermic cause

HYPOTHERMIA (lower than normal temperature)

How to recognise it --> Body temperature <37 degrees Celsius, critical temperature 32 degrees Celsius 

What causes it --> Anaesthesia! 

How to fix it --> Provide passive warming (towels, blankets) and active warming (bair huggers, hot mats, warm water bags).

ARRHYTHMIA (abnormal heart rhythm)

How to recognise it --> ECG, auscultation, pulse deficits present 

What causes it --> Inappropriate anaesthetic plane, hypercapnia, hypoxaemia,  hypotension, hypothermia, medetomidine, electrolyte or acid-base abnormalities, cardiac disease

How to fix it --> Maintain adequate anaesthetic depth, atropine for sinus arrhythmia (bradycardia) only if BP affected too, oxygen and IPPV, stop drug administration, lignocaine bolus or CRI, fluids, warming 

HYPOTENSION (decreased blood pressure)

How to recognise it --> Systolic arterial pressure (SAP) <90 mmHg, Mean arterial pressure (MAP) <60-70 mmHg, arrhythmias, tachycardia

What causes it --> anaesthetic drugs, too deep anaesthesia, hypovolaemia, heart disease, arrhythmias, organ manipulation, IPPV capillary occlusion

How to fix it --> Adjust anaesthetic depth + use MAC/dose-sparing adjunctive drugs, fluids, atropine if bradycardia, dopamine CRI or ephedrine bolus (positive ionotropy)

HYPERTENSION (increased blood pressure)

How to recognise it --> SAP >160 mmHg, MAP >140 mmHg

What causes it --> Too light anaesthesia, painful stimulus, drugs such as ketamine, hypoxaemia, cardiac disease, renal insufficiency, increased ICP (Cushing’s reflex - increases MAP)

How to fix it --> Deepen anaesthetic plane or provide analgesia, IPPV/PEEP and oxygen, wait for hypertensive drugs to wear off, mannitol or furosmide if bradycardia too (increased ICP)

HYPOVOLAEMIA (relative or absolute decreased blood volume)

How to recognise it --> monitoring blood loss during surgery, pale mucous membranes and increased capillary refill time (CRT), tachycardia, hypotension, increased apparent depth due to reduced cardiac output to lungs 

What causes it --> Relative (vasodilation) and absolute (blood loss, dehydration)

How to fix it --> Minimise inhalant use with MAC-sparing agents such as opioids as well as close depth monitoring, fluids, positive ionotropy (dopamine e.g.), calcium, keeping the patient warm 

APNOEA (not breathing)

How to recognise it --> patient not breathing, flat line capnograph

What causes it --> Post-induction (light plane anaesthesia), drugs (propofol e.g.), too deep plane of anaesthesia, lung pathology, paralysis 

How to fix it --> IPPV and oxygenation, analgesia, manage anaesthetic depth closely

TACHYPNOEA/ HYPERVENTILATION (breathing too fast)

How to recognise it --> Respiratory rate >20 breaths/min in cats and 30 breaths/min in dogs

What causes it --> Light plane anaesthesia, painful or strong stimulus, hypercapnia, hypoxaemia, hyperthermia, weak respiratory muscles, abdominal enlargement 

How to fix it --> Deepen anaesthetic plane, provide analgesia, oxygenation +/- IPPV, active cooling, optimal patient positioning 

HYPOVENTILATION (breathing too slow/shallow)

How to recognise it --> ETCO2 >55 mmHg, apnoea/bradypnoea/shallow tachypnoea, brick red mucous membranes, tachycardia, increased blood pressure, tidal volume <10 ml/kg

What causes it --> Too deep in anaesthesia, drugs (e.g. inhalants, propofol), poor positioning, large abdomen, thoracic pathology, paralysis, rebreathing, open thoracic surgery 

How to fix it --> Oxygenation, IPPV, and reducing depth 

HYPOXIA (low tissue oxygenation)

How to recognise it --> SpO2 (pulse oximetry) <90-95% or PaO2 <60-80 mmHg, bradycardia, cyanosis, cardiac arrest 

What causes it --> Too deep anaesthesia, rebreathing, inadequate oxygen flow rate, airway obstruction, V/Q mismatch (pulmonary shunt), hypovolaemia, cardiac failure, hypoxaemia, shock, cyanide toxicity, anaemia

How to fix it --> Assess airway, oxygenation, lighten anaesthesia, IPPV, positive ionotropy (dopamine e.g.) if cardiac failure, fluids, check your anaesthesia set up

PATIENT TOO LIGHT 

How to recognise it --> positive withdrawal reflex and palpebral reflexes +/- blinking, tachycardia, hypertension, tachypnoea, movement with stimulus, swallowing/ chewing/ salivation, central dilated pupils, 

What causes it --> Low vaporiser output, low flow rate, inadequate ventilation, rebreathing, disconnected circuit, ET tube too long (only one lung gassed down), leaks

How to fix it --> Check the anaesthetic circuit for disconnection, excessive dead space, or leaks (should be done prior to every anaesthesia), icrease vaporiser output, increase flow rate, change ET tube, IPPV

PATIENT TOO DEEP

How to recognise it --> weak jaw tone, central dilated pupils, reduced or absent palpebral reflexes, withdrawal reflexes, and ear flick (cats), bradypnoea and reduced tidal volume, hypotension, pale mucous membranes + increased CRT, no response to strong stimulus 

What causes it --> Low cardiac output, high vaporiser output, hypothermia, poor depth control/complication troubleshooting

How to fix it --> Disconnect the patient, turn off the vaporiser, and flush the system through with oxygen via squeezing and refilling the rebreathing bag, connect to the patient with pure oxygen, warm the patient.