#10 Thyroid Disorders

Before we get into this episode, just to mention, always wash your hands, always gain consent, and aim to ensure that a patient's welfare, safety and comfort is maintained throughout the exam. This podcast is supported by Past Test. Past Test is an excellent resource which has a vast library of photographs, videos and notes which you can use to help prepare for the exam. For ice-based candidates, you can also claim back the cost of the resource using the training support scheme. So welcome back to MRCPI bedside. Today we're joined by Dr. Michelle Mahar. Dr. Michelle Mahar is an endocrinology, SPOR working in Dublin. Thanks Michelle for joining us today. No problem on delighted too. And today we are going to talk through an endocrine case and the case that we're going to discuss is going to be the thyroid exam, which is something that comes up quite commonly in its scene in Station 3 of the short cases of the MRCPI clinical exam. Yeah, absolutely. And it's a really common one to come up, so a good one to have a good approach for. We might just start by talking through your approach to an exam. Yeah, absolutely. And so as you mentioned, Christine, Station 3 tends to be kind of an endocrine case, but it's open to kind of miscellaneous examinations, but more frequently you might come across a thyroid case, for example, or acromegyl or a diabetic foot. Sometimes it might be a little bit less clear from the instruction what kind of exam you will be asked before and what the examiner will always guide you. For example, in the case of acromegyl, they may ask you to eyeball the patient first and then proceed with the examination as acromegyl is more of a spot diagnosis. And then in the case of thyroid disease, they might ask you to examine the neck to start off with the eyes and then ask you to proceed from there. So it's all about a spot as remaining calm for the first few minutes and just proceeding as you see fish and the examiner will always guide you and you will go completely down their own route. So how would you approach the exam? So from the thyroid perspective, I suppose you'd always start with your general inspection, so you'd probably be hoping that the patient isn't going to be overtly, the thyroid toxic for the point of the exam, but they might have more features of an established diagnosis of Graves disease, for example, or thyroid surgery or thyroid eye disease. And I think for the purpose of this, we might focus on the exam as it relates to the thyroid toxicosis as opposed to hypothyroidism, which is probably pretty rare that you'll be asked for as a shortcase. But I suppose just to get back to the exam, you probably aren't going to find major features of thyroid toxicosis by looking at the person, but in general, you'd be looking for things like the person being tremulous or restless and that they have evidence of heat intolerance and might be wearing a little in way of clothing. And then you'd move on to looking at the hands, looking for any evidence of tremor, sweating or panorathema, which be consistent with thyroid toxicosis, looking for evidence of thyroid acropathy, which is similar to clubbing, and it's quite rare, but it's specific to Graves disease. And then obviously assessing the pulse, looking for evidence of tachycardia, and particularly atrofibrelation. And then importantly moving on to the face and most importantly the eyes. So I think it's really important to exaggerate the eye examination and look at the patient from all angles, including from the front and the side and the back. So looking for evidence of exothalamus, looking then for evidence of lid retractions that you could see the whites of the eyes, either side of the iris, when just looking at the eyes, and then looking for other elements of more active thyroid eye disease. So periorbital edema, swelling around the eyes, and tearing or redness or erotema of the conjunctive, which is conjunctive, which is conjunctive, for ejection. And then to assess the eyes further you'd ask the patient to follow your finger and assess their eye movements. So looking for the range of their eye movements, asking if there's many pain or doppel vision. And also performing lid lag. I suppose moving on from the eyes. Then next most important feature of the exam will be the neck. So just looking at the neck, first of all, there may be glass of water beside the patient asking them to swallow. So that's one of the main kind of pointers to the thyroid exam that you might see next to the bedside table, and there's kind of a prompt to, you know, that's what you're going to be doing is going to be a neck exam and goysia exam. Exactly. Yeah, exactly. So you're looking there to see that the thyroid moves down and swallowing, and then moving into, to perpetre the thyroid gland from behind and assessing the size and the nodularity of it. So in the case of graves disease, you might have a diffuse enlargement of the thyroid gland, but in the case of a multinodular goysia, there might be more fork areas of nodularity. And then as further points, you can percuss the gland, looking for evidence of retrasternal and dullness, and you can also listen to the gland, then look at listening for a burie, which can be specific. More so to graves disease and indicates a hypervascular thyroid gland. And then I suppose for completion, you could say that you might complete pembert and sign if you were concerned about a retrasternal goysia, that was causing compression of the trachea, but it's unlikely that that's going to be the case in the exam. For those of us out there, he don't know what the pembert and find is, how would you listen to that? Yeah, so you just asked the patient to put their arms up over their head and hold them there for at least 15 seconds and looking for any evidence of strider or that their face is becoming engoriant and red as well. Great, thanks a million. No problem. And I suppose that would be the main focus of the exams, really kind of focusing on that general inspection behind face and the neck, but you could say for completion that you would look for other signs, which might include pre-tibial mixidema, which is quite rare again, but supposedly a kind of waxy discoloration of the shins that happens at graves disease and then looking for evidence of proximal myopathy and assessing the reflexes, which might be increased in pyrotoxicosis as well. Am I right in saying my experience and from what I've heard from other exam candidates in the past is that often the exam there is kind of trying to tease out from you if you have identified any active signs of thyroid disease and yeah, you've gone through them quite nicely there. So, what are those specific signs would indicate active disease? Yeah, I think probably one of the most indicative ones is probably the tachycardia or naturophypilation, but someone that's maybe flushed or has a tremor for example, that would be another area that you could assess and then obvious sweating or diaphrases as well maybe. That's a really thorough exam for patient with pre-symthoryrae disease. So then I'm moving on to kind of a differential for a neck mass or what would you kind of, what would your tap differentials be? Yeah, I suppose it's just word-be-mindful that all the way we're talking about the thyroid, there could be other kind of neck masses. So here you might be more focused on a goitre, which is a midline mass related to the thyroid, but you might include in your differential the lymphadenopathy, which can occur really anywhere in the neck and might be a reflection of acute infection or something more sinister or systemic like lymphoma. Also common skin lesions like polmas or sepacias cysts for example, or maybe rare rottings then like vascular malformation of the crotted for example. So then I think that kind of leads us on to talk about goitre specifically and causes of a goitre. So could you talk us through the causes of a goitre, Michelle? Yeah, no problem at all. So I suppose the most common cause really would be the goitre of braids disease, which is typically a diffuse enlargement of the thyroid gland and it's smooth and you might have that thyroid brie like we talked about. Another really common cause would be multinodular goitre and these are often seen in more elderly patients. So that means that rather than the gland being smooth, it's more nodular and you'll be able to have palpate individual nodules. It's also possible then to have a dominant nodule or maybe a single nodule as a result of a single adenoma. And then you may just have a simple goitre in the absence of having underlying thyroid disease or such or underlying thiochoxicosis, which might get in current regions that have low iodine levels, for example. Graves disease is indicative of hyperthyroidism. What other causes, primary causes of hyperthyroidism are there? Yeah, so absolutely graves would be the most common cause and particularly in younger people, generally in women who present in maybe their thirties. But there are other causes. So a toxic multinodular goitre can produce thyroid hormone, for example. And again, this may be in the older patient, a toxic adenoma can also produce excess thyroid hormone. Medications are an important one. And if you're encounter this in the long case, it would be good to ask a good medication history. So things like amyodron, e, for example, and even if patient is previously taken amyodron and is now not taking it, that can cause a thirtocytosis because it has a really long half life. And then other things like contrast media from CT scans or I suppose rare would be if someone was taking L-truxin, so for kind of a fictitious thirtocytosis. And then I suppose the final big cause. would be a thyroiditis as well. Yeah, and so they'd be the main kind of primary causes of thyroid oxychosis, but of course you can have secondary causes which would mean that the TSH is elevated and that's driving the thyroid hormone up, but these would be a lot more rare and would include things like a TSH Oma from a Pituatri tumour. Great Michelle, that's fantastic. And then I guess investigations of a goisher or in the patient, in this core as a patient, how would you start? Yes, so of course you want to get your thyroid function tests, so these would generally include a free T4 and a TSH or a thyroid stimulating hormone. And in thyroid oxychosis you'd expect the free T4 to be elevated and the TSH to be suppressed, and that's in cases of primary thyroid oxychosis which were probably largely focused on. It's also useful to get a free T3 as well because sometimes a patient might have a normal free T4 level but a suppressed TSH, but they might still have an elevated free T3 and be thyroid toxic biochemically. So that would be the starting point definitely. You then go on to do a TSH receptor antibody which is a really useful test because this is reflective of Graves disease and is positive in the vast majority of cases of Graves disease. And that sort of clinches your diagnosis then and means you don't really have to pursue further imaging and things like that. TPO antibodies can also be sent but are very non-specific, they're reflective of auto-immunity and generally occur in Hashimoto's tireditis for example, but they're not particularly helpful however patients often have them sent before even coming to clinic. And then I suppose your routine bloats are important as well, so an FL blood count looking at the patient's white cell count neutrophils. This is important because Graves disease can cause a neutropemia baseline but also some of the medications which we'll talk about can cause a neutropenia as well. And then to get baseline liver function tests is also important because again some of the medications can cause deranged LFTs and be hepatotoxic but also in the tired toxic state people can have deranged LFTs as well. And so they would be the most important ones of the routine bloods but also worth just performing a full routine panel checking the renal function and calcium levels as well. And moving on from blood tests, what would your goal standard of imaging be for patients with these signs? So sometimes imaging might not add a lot and may not be necessary, particularly if the patient fits for a Graves disease both in terms of their clinical presentation and their biochemistry but it can be useful particularly where there's a goi-sure or where there's evidence of nodules more so an ultrasound of the thyroid scan will help you to find those nodules and they are given a score by the radiologist which is called a T-RAD score and that indicates how you need to proceed with them and whether you need to biopsy them if there's any concerning features for example or whether they look like they could particularly be a crycinoma. So that would be probably the most useful form of imaging. Sometimes a radioisotope scan can be useful if you're unclear about the diagnosis for example or it's not possible to do a biopsy and there's a concern about an underlying cancer and that you'd be looking for the optake of the or the pattern of the radioisotope scan so in Graves disease you'd expect a diffuse uptake of the tracer whereas in a multinagilar goi-sure you might see more focal areas of uptake and then entire diagnosis you wouldn't see any uptake at all for example. You could consider doing a CTN X and TORACs if you're concerned about a very large goi-sure that was maybe compressing the trachea as well but this probably wouldn't be necessary for the vast majority of cases. Great. Moving on to treatment options for Graves disease. Where would you start? Yeah and I suppose the main focus of the management is really Graves disease because that is the majority of cases of thyrtoxacosis and some of the other forms of thyrtoxacosis will have more individual management but I suppose the starting point for Graves would be to treat with antithyrid medication which is generally carbimazole and this is titrated according to the starting thyrifunction test generally they're free T4 and the dose then is adjusted as they respond to the medication and their TFTs respond. So this works by inhibiting the synthesis after thyroid hormone and generally it's given for 18 months and then prior to stopping therapy at a TSH receptor antibody would be checked and the TFTs as well and you would probably only stop the medication if the patient was uteroged and their TSH receptor antibodies were negative as if they still quite high this indicates a high chance of relapse and there is a very side effects associated with carbimazole. So the most common is probably a rash can also be a patotoxic and cause drainage del FTs and then one of the ones people are generally more familiar with is the risk of agranilosythosis or neutropenias so what you consider neutrophils maybe below 0.5 and again this can occur in about one 500 people generally occurs in the first couple of months of treatment and it's not you can't really predict when it's going to happen so there's no use essentially of monitoring full blood counts because it can just occur acutely but I suppose it's just important to counsel the patient about this and if they develop a sore throat or a fever to get their blood checked for a full blood count and then I suppose in terms of symptomatic management generally we would give long acting beta blockade with propanolol as well and this can be down titrated as the patient responds symptomatically. And specific to the management of thyroid eye disease where would you start with your management for those patients? Sure so I suppose it's important to assess house veer at the thyroid eye diseases so in some patients they might have quite mild symptoms and these could be managed with more topical measures such as lubricating eye drops for example. It's important to establish if the patient has any visual loss as this requires an urgent referral to ophthalmology absolutely and in case of more moderate to severe act of graves or a thyroid eye disease and the patient really will need pulsed IV methyl prednisolone therapy which is a course of weekly infusions of methyl prednisolone generally up to 12 weeks and if this doesn't work there are second line agents so various immunospressons like retoximab or cycus borin can be used in conjunction with steroids and there is a new monoclonal antibody therapy as well called depertumamab but I'm not sure if that's actually been actively used at the moment and generally IV steroids are probably the main state of severe eye disease and of course urgent decompression of the orabish if there is very severe optic neuropathy that's not responding to steroids. Am I right in saying that one of the big things with management for eye disease is smoking cessation? Absolutely yeah yeah so 100% and it's really important to cancel patients about this as well and of course to mention as well patients with tired eye disease are limited in terms of further options for treatment and that generally they wouldn't be considered for radioactive eye dying therapy as well as this could exacerbate thyroid disease. Michelle apart from education are there any other management options for these patients? Absolutely so the two major forms of definitive treatment are either radioactive eye dying therapy or surgery with a total tiredectomy so I suppose there's a lot of considerations into which therapy might be opted for but radioactive eye dying therapy is sometimes an attractive option because you avoid surgery however it does involve administration of an oral radioactive tablet and patients can't be around children or example for a period of time afterwards so it might not suit young women who have children for example and it can exacerbate tired eye disease as well so patients with moderate to severe tired eye disease wouldn't really be handled it's for it. Surgery is also a definitive option and a lot of patients can opt for this as well particularly if they have a large geyser and want to for cosmetic reasons or if they have a goiter that's causing compressive symptoms for example and then also if if they've trialed anti-tired medications this just failing to work and Michelle am I right in saying that radioactive eye dying and surgery is usually for patients with kind of solitary toxic nodules or a multinodular goysher and graves is kind of further down the list? Yeah sure absolutely like in graves disease generally you'd consider a trial of anti-tired medications in the first instance but if a patient for example is a really high TSH receptor antibody or they're not responding to anti-tired medications at all in the first instance then you might have to consider earlier definitive treatment. That was a great run through thyroid disease and I don't think there's anything else to add thank you so much Michelle for joining us this evening and Michelle has taken time out of her busy work schedule to join us on a gorgeous sunny evening so thanks Michelle no problem I'm already delighted too. A big thank you again to stepping on Lego who provide our amazing show music if you'd like to get in touch they can be contacted at steppingon [email protected] or through social media and if you want to contact us you can get on touch via our Instagram @mrcpi bedside twitter account or ex-account @mrcpi bedside or email which is mrcpi [email protected] thanks again and good luck. Good luck