Hi everybody, I am Gina Parks. Thank you for joining me with the webinar vet for this two part series on endocrine nursing, with part one focusing on understanding endocrine disease. So the learning outcomes for part one and part two are to refresh your knowledge of the anatomy and physiology of the endocrine system, mostly just focusing on some main organs that are affected in endocrine disease and what hormones are involved in those diseases.
We're gonna try and refresh ourselves about the hormones that are involved in maintaining homeostasis. And then in this part one session we will continue on to start to cover some of the common endocrine disorders in veterinary patients and hopefully by the end of this session you'll be able to recognise. Some of those, and then as we move on to part two, we will continue to cover some of the common endocrine disorders, and what those are about and sort of refresh our understanding of those, and then we'll go on and discuss some diagnostic approaches for those being hyper and hypoadrenal corticism patients, and then we will carry on and evaluate some nursing care priorities, particularly focusing on, Hyper and hypoadrenal corticism disease patients, so, looking forward to covering all this material with you over the next two sessions.
So when we think of the endocrine system, then what do we think of? So the endocrine system is the name given to the main body system that is responsible for maintaining metabolic homeostasis in our patients. And it's composed of a series of glands which are located around the body, which are responsible for sending chemical messenger signals and we call those messenger signals hormones.
What is a gland then? So a gland is just a group of cells or tissue that secrete a substance, and you might remember from your undergraduate studies that there are two types of gland in the body, exocrine and endocrine glands. With exocrine glands secreting a substance that's already active directly onto the area that it's needed, such as saliva, whereas endocrine glands, which are the glands that we're concerned for the purposes of these sessions, secrete tiny amounts of hormone into the bloodstream.
And then these hormones travel off to other parts of the body, and they attach to receptors in or on the cells to cause change. So what do we mean by a hormone then? So most animal hormones are made from small proteins which are a series of polypeptides or steroids which are essentially for carbon atom rings.
So the molecular structure is very similar between steroids, you'll see on the page there, there are. Some names for steroids that we're quite familiar with, especially in adrenal patients and, endocrine patients. So cortisol, corticosterone, aldosterone, cortisone, progesterone, and testosterone are all made from a similar structure.
All being that 44 carbon atom ring makeup with progesterone and testosterone being more associated with the sex hormones, we quite commonly will come into contact with cortisol, cortisone, corticosterone, and aldosterone problems in patients with endocrine disease. And virtually all cells in the body receive signals from different hormones and respond appropriately, with too much of a hormone being typically classed as a hyper condition. And too little of a hormone being classed as a hypo of a condition.
And when we think about the endocrine system, if we imagine that the body is an internal post office, then the endocrine system could be the internal mail system that works in the body. So if you think about these tiny hormonal letters that are being sent all over the place. And if the mail system goes wrong, goes on strike, or starts to deliver the wrong amount of letters to an address, then there's chaos, and it's the same with hormones and and the endocrine system.
And if the body is the post office, then the main glands that we would consider addresses include the pituitary, the thyroid, the pancreas, the parathyroid, and the adrenals, and the sex organs. We're not going to cover diseases that affect the sex organs at all in these two sessions, but it's worth noting that they are included as part of, endocrine organs. So when we think of endocrine diseases in our canine and feline patients, then what are the ones that we're seeing most often?
So the most common endocrine disease that we will see is feline hyper hyperthyroidism, with about 1 in 10 cats suffering from it. Canine and feline diabetes is next, with about 1 in 300 dogs and or 1 in 250 cats, which blows my mind a little bit because I feel like that, we see more of them than that, but that's what the figures are, that's what the statistics are. Canine hyperadrenal corticism then with about 1 in 360, and canine hypothyroidism with about 1 in 400, and canine hypoadrenal corticism with about 1 in 1600.
And then lesser commonly than that, we will see hyper and hypoparathyroidism, sex hormone imbalances, diabetes insipidus and other endocrine diseases such as thyroid tumours, etc. But they are much less common. So for the purposes of this session then, we'll start to touch on some of these more common ones and just give a brief overview of the ins and outs of those diseases.
OK, so let's start with diabetes then. So diabetes mellitus is defined as persistent hypoglycemia and glucosuria due to an absolute or relative insulin deficiency. So by relative what that means is that it can be enough to cause the problems associated with having an insulin deficiency.
There's different pathophysiology in cats versus dogs, so we'll look at that in a little bit more detail now. So in dogs then we liken that to type one in humans where there is damage to the eyelets of Langerhans with the beta cells in the pancreas, meaning that there's lack of insulin production via an autoimmune disease, so where the body starts to attack the pancreas itself and damage those cells, and that's progressive in dogs, so it's important that we know this as nurses because we need to be able to support clients on the pathway that they're gonna go down with care. And we'll look at that in session two, of this two part series.
But this is a progressive disease, the patient's not going to get any better, they're not going to be able to go into remission, and they're likely to need continuous and increasing replacement of insulin. So they are insulin dependent, and this is the, the type that most dogs will get. In cats then we liken their disease to more like type 2 diabetes in humans.
Which is essentially a combination of two factors playing a role, so partially functioning beta cells, which are only partially and abnormally secreting insulin. And potentially not secreting very much, and then we combine that with poor lifestyle, that some cats have, which causes increased peripheral insulin resistance, and it tips them into diabetes, and it's important as nurses we understand the difference in cats and dogs because if we get the lifestyle under control in some cats and we stop overfeeding and stop contributing to their peripheral insulin resistance, then the beta cells that are there, they can actually function. And so we can actually tip these cats back into remission with with careful and early insulin therapy.
So it's, it's important as nurses that we understand the differences in the two disease processes so we can support the client and and ensure that we help them on the right care pathway. And then it's also important for us to understand that there's a small cohort of cats that actually potentially don't have that disease process at all, but their diabetes is driven by a condition known as hypersomatotropism. So some studies suggest that as many as 1 in 4 diabetic cats can actually have this brain tumour essentially, which is causing excess production of, Growth hormone in the somatotrophs of the anterior pituitary gland, which is actually leading to insulin resistance, and there is only one cure for that, and that is to have that tumour removed, the treatment of choice for that would be hypovasectomy, and with these cats, the insulin would, the requirement would increase continuously as the tumour grows.
And the the patient would just be sicker and sicker and so it's important for them to be tested for excessive growth hormone with a blood test. But how are diabetics presenting then? So if we think about what diabetes is, it's an inability for glucose to enter the cell, so patients aren't going to have any energy.
And as they try and obtain energy, they're going to try and eat some more food. They're potentially going to have excess glucose crossing the renal threshold in the kidney and dragging with it some water. And so these patients are going to present as polyuric and then the subsequent polydipsia to replace the water.
The client's often going to come in and say that they've got behavioural complaints regarding urination because potentially the animal is now urinating frequently in the house, outside its litter tray, maybe potentially, you know, it could be a well behaved animal before, very well toilet trained animal, and then all of a sudden they're coming in with urination problems. They might present with polyphagia if the disease is early in in sort of earlier on and the animal's not too sick. Obesity, weight loss, and then as the disease progresses and their body starts to break down other sources of energy for other sources of energy stores for, for energy, then the, the animal could have fat pattern muscle loss.
You do see these poor animals coming in with really severe muscle loss along the back and then this sort of fat sort of potbelly appearance. Urinary tract infection, inappotence, and dullness and lethargic as well. Diagnosis is fairly straightforward with the vet requesting a blood sample and the blood sample being elevated for fasting hypoglycemia, so outside of the normal blood glucose range.
These patients might have a bit of a stress response going on, so they might have a leukocytosis. They will often have elevated liver enzymes as the liver tries to process the excess fat that's been broken down and also the glucose, the elevated glucose in the bloodstream is actually causing potentially some. Glucose toxicity.
The kidneys are working really, really hard at the minute as well, so the patient might have some azotemia. We will quite commonly and and very indicatively see a glucoseurea as the the glucose spills across the renal threshold. And the vet might ask for other blood samples that will rule out other causes for hypoglycemia, which we know, hyperadrenalcorticism, stress, things like that can all cause elevated blood glucose levels as well.
What's really important to know is that we are not aiming for this patient to be normal glycemic, so these patients have been diagnosed with diabetes and to be normal glycemic is actually a little bit too close for comfort, too hypoglycemia for us. So we're aiming to alleviate clinical signs and allow a good quality of life for both the pet and the owner. So we're quite often aiming for a blood glucose concentration.
Of around 5 to 12 millimoles in dogs and 5 to 16 millimoles in cats, the risk of a hypoglycemia when we aim too low is, is potentially deadly and so that's not something that we want to do. OK, so let's move on to the thyroid then because we've still got a lot to cover in this session and we're not even halfway through yet. So, OK, the thyroid then is a bilobed gland which is sits in the caudal larynx of the lateral trachea.
It consists of follicular cells of secreting components with a colloid storage centre surrounded by thyroid epithelium. And it responds to the pituitary gland producing thyroid stimulating hormone, and in response to thyroid stimulating hormone, it produces thyroid hormones T4 or thyroxine and T3 triiodothionine and calcitonin as well. So calcitonin we know is responsible for helping maintain normal calcium levels, and then we have T3 and T4 with T3 consisting of three iodine atoms, being a potent hormone that's used in the liver and the brain, which helps increase oxygen consumption.
And T4, which is 4 d matoms, being present in the bloodstream in two forms, and this is something that I don't think as nurses anyone ever explains to us. So it's T4 exists in bound and free, so bound or non-bound, bound or free. Bound T4 is attached to a protein, so it's preventing itself from being used up, it's circulating and acting as a reservoir, it's basically unable to enter any target tissue, so it's basically a backup supply.
And then free T4 is available to enter target tissues, that's the amount of active T4 that's in the body that's available to be used. T4 increases production of adenosine triphosphate or ATP, which is an energy carrying molecule, so it causes an increase in basal metabolic rates. Whenever we have an increase in in metabolism.
We have an increase in carbohydrate and lipid breakdown for energy, so T4 essentially causes carbohydrate and lipid breakdown. To be increased, it's ionotropic and chronotropic, which means it increases cardiac output, and it also increases adrenergic receptors in skeletal muscle, adipose tissues and lymphocytes as well. So let's look at that in a little bit more detail now.
So let's look at this in a little bit more detail then, I'm just going to get my laser pointer here, so this is the negative feedback system that's associated with the the thyroid gland. So what we have is the hypothalamus in the brain producing thyrotropin releasing hormone, which stimulates the pituitary to produce thyroid thyroid stimulating hormone or TSH which stimulates the thyroid to produce T3 and T4, which we've said causes increased cardiac output, is ionotropic and chronotropic. Increased metabolism, increased intestinal food processing, patient temperature, everything to do with metabolism will occur, will increase with increased T3 and T4.
And then when the levels get to a high enough point, what would happen is the hypothalamus would cut off the production of the TRH and stop producing, stimulating the pituitary to produce TSH, which would stop stimulating the thyroid. When the levels drop because they've been used up by the cells and the levels have gotten down to a low enough level that we need more, then the hypothalamus would sense that and it would kick in and release more TRH and the process would start again. So let's look at the diseases associated with the thyroid then.
So the first one is gonna be feline hyperthyroidism, where we have too much T4 and as we just said, when you have too much of T3, T4, then we have an increased heart rate, metabolism, increased carbohydrate, protein and fat breakdown. And it's caused by nodules developing within the thyroid gland which spontaneously excessively secrete thyroid hormone. So essentially it's not listening, the thyroid is not listening to the amount of TSH that's being produced or not produced by the pituitary.
It can be caused by hyperplasia or adenomatous changes, less commonly carcinoma, but we do see carcinomas in cats, with sort of longer standing hyperthyroidism. The excessive secretion of thyroid hormones has a negative feedback effect on TSH production, so classic endocrine test results of a feline with hyperthyroidism are increased T4 and suppressed TSH levels. So let's look at that in a little bit more detail then.
So this is our negative feedback system and what we said in a healthy patient is that when the levels get to a high enough point, in the bloodstream and in the the hypothalamus can sense it, it will cut off the TRH to the pituitary, which will cut off the TSH to the thyroid. However, cats that have too much T3 and T4 because they're hyperthyroid are not listening to the pituitary. And so cats that have hyperthyroidism will have a high T3, T4 and a low TSH because the TSH.
Has been cut off because the hypothalamus and the pituitary feedback system has worked, but the thyroid's not listening, and so it's continuously continuously pumping out T3, T4, which is causing this increased metabolism. And essentially all the the organs are affected and the feedback system's flooded, but cats will often have a high T3, T4 and a lower TSH. So treatment options then, so actually a diagnosis of feline hyperthyroidism without intervention is fatal, which I think people forget because we're so used to treating it now.
But treatment does increase survival time substantially from potentially as low as 2 years to more than 5. So we do have options for treatment with anti-thyroid medication, surgical thyroidectomy, radioactive iodine therapy, and iodine restrictive diets being the most commonly sought after for treatments. So we'll just look at those in a little bit more detail now.
Anti-thyroid medication then is probably the most common type of therapy that we give to our hyperthyroid kitties. They are useful, they decrease the production of thyroid hormone and can reduce the clinical signs associated with really high levels of T3 and T4 quite quickly, so those signs associated with thyroid toxicosis, you know, having a very high metabolic rate, tachycardia, you know, abnormal functioning GI tract. Hyperactivity, all of these things can be, you know, well controlled using these medications.
Methimazole is the most common, probably one that's given with about 2 weeks to eut thyroidism being achieved, when given orally, or transdermally about 4 weeks. We have to be really careful with this because owners are obviously sensitive as well to the drug being transdermal, so we don't wanna make anybody hypothyroid by giving transdermal without using gloves. And then the other one is carbimazole, which is a prodrug, which is used, probably slightly less commonly than methimazole just because of the side effects that we'll go into in a second.
But it's converted to methimazole within the body, so it takes a little bit longer to work, so it's about 4 weeks to, to reach your thyroidism. All doses have to be tailored to the cat's disease and the severity with close monitoring required, . For about 3 months, and the 1st 3 months is when the most common side effects occur.
The side effects then that we said we would discuss are associated with quite a high mortality rate as well, which is unfortunate, but there's two groups really, so the common less severe side effects would be GI signs, nausea, vomiting, lethargy, diarrhoea. Leukopenia, eosinophilia, lymphocytosis, facial excoriation caused by scratching puritic skin as the cat on the screen shows, and it's not really that uncommon that I see this in the cats that are in the radioactive iodine unit that I work in. So it definitely is something which many patients will have to convert to another therapy due to.
And then the less common but the more severe side effects which can lead to quicker fatality would be those associated with thrombocytopenia, hepatopathies, severe leukopenia, haemorrhage, and clinicians are advised to stop all anti-thyroid medication if any of the side effects really are noted anyway, and to think about potentially taking a different route. We can also cause iatrogenic hypothyroidism if we are to go too heavy on the dose or to maintain the dose for too long without checking that it's the right dose, so that's something to be aware of as well. So you might be wondering then why clinicians start cats on those medications knowing that list of side effects to be quite extensive, but I guess they're still probably less upsetting than the side effects of being hyperthyroid and we did say that hyperthyroidism itself is is fatal, so.
Definitely worth trying them on medications, not every cat has side effects. They are less costly to the client per day than some of the other treatments. They unfortunately are a a lifelong commitment.
As soon as the the animal stops having that medication, then the thyroid levels will increase again. The thyroid will still be overactive and so we'll still increase the levels of T4 in the in the bloodstream as soon as we stop the anti-thyroid medication. We do have to explain to clients that there's repeated vet's visits required for those sorts of medications to make sure that the, the dose is correct.
We're not overdoing it, but we're also not underdoing it as the disease progresses. It's a tumour, it probably will grow and the dose will need reviewing and adjusting. But the quality of life is generally less stable than the other options as well, and not all cats are amenable to having a tablet, so it's certainly worth noting that whilst being a very common medication, it's not always the right one.
So surgical thyroidectomy would be another commonly carried out procedure for hyperthyroid cats where a skilled surgeon removes the hyperplastic tissue to to treat the hyperthyroidism that way. Does cost more than the medication in one sort of large amount but. I guess if you were to add up the amount of medication over the the period of the cat's life, I'm not sure that there'd be that much difference.
The wound does need some aftercare and there's always associated an anaesthetic risks with any surgery. But yeah, we can stable cats by putting them on anti-thyroid medication prior to treatment which will make the anaesthetic risks a little bit better. So surgical thyroidectomy is definitely an option.
Huge thing to be aware of is that tweaking or damaging the parathyroid glands can result in postoperative hypocalcemia, which then could require vitamin D and calcium supplementation for quite a long time afterwards and does need a lot of close monitoring. And hypothyroidism following the removal of the whole gland does mean that then we would need to supplement with thyroid medication. But the thyroid medication is generally a little bit easier on the body because you're just supplementing with a hormone that's missing, so it's a little bit easier to give than the anti-thyroid medication, it's a little bit nicer on the body.
Radioactive iodine therapy then is my favourite therapy for hyperthyroidism, primarily because it's what I do for my role, mostly in my job and also because it's so successful for our hyperthyroid cats. So thyroid hormones and thyroglobulin are the only molecules in the body that are made using iodine. So that means anything ingested or injected will be taken up by the thyroid and used in the production of thyroid hormone.
So why is there a mouse on the screen? I can probably hear you say, well, we'll chat a little bit about that in a minute when we come to the diets that are involved in treatment of hyperthyroid cats. So within a radioactive iodine unit then, iodine, it's particularly iodine 131, radioactive isotope is injected into the subcutaneous space under the skin of a cat, or it's contained within a pill that is given orally, and it then concentrates within the body in the thyroid.
So beta and gamma particles from the radioactive isotope then start to destroy the hyperplastic thyroid tissue, and as I said, it's very successful. With about 95% or more, success rate in our hyperthyroid kitties. So the pros of it then are that it's, as we said, very successful, no more medication needed, very minimally invasive, it's literally a subcutaneous injection or pilling a cat, potentially with a little bit of mild sedation, just so they don't bite down on the capsule.
There are very few complications associated with this therapy. You don't have any surgical wound to sort of have the patient recover from, there's no risk of infection, there's no risk of breakdown, so that's a real big plus. And then I think if we look at the cost long term versus medication, then it actually can be quite a useful thing to do in regards to cost.
Yes, again like surgery, you might have a large outlay in one go, but. After that then kind of you don't have any further costs, and when you look at medication given over a length of time it can total up to not that not not that dissimilar an amount. So cons then to give a balanced view would be that the patient usually has to be hospitalised for a period of time and the ones that I see are hospitalised for about 12 days.
They can require restraint, so patients which are not used to or do not like to be restrained in any way, shape or form are not gonna be er very happy with this procedure and may need to be sedated. Er it can become more expensive if the patient requires additional support during hospitalisation for any reason. It can become more expensive I suppose if a patient stops eating and needs, you know, appetite stimulants or other things which cost money.
It does cost more in one, in one go, the medication, as we said, and it's not effective in all cats because some may require another dose. So we did say it was about 95% or more successful, but that does mean 5% of cats potentially it wouldn't be enough, and that's because the thyroid tumour is too large or potentially they have a carcinoma or something like that which we didn't know about and they need a higher dose. And then in some cases unfortunately the thyroid hormone can actually go a little bit too low, so feline hypothyroidism, iatrogenic hypothyroidism can actually cause poor renal blood flow, so we would have to then give those patients supplementation with.
Hormones replacement, essentially thy thyroid replacement hormones, because we, the, the, the tissue's never recovered and we've left them with iatrogenic hypothyroidism, and that is something which is a risk factor in in patients which have potentially poorer functioning kidneys, because persistent poor renal blood flow can actually cause further kidney damage in those cats. And then iodine restricted diets are the 4th choice of care for these hyperthyroid cats with these diets being very, very, very restricted with iodine. So we said, didn't we, that production of thyroid hormone can't occur unless the patient has some intake of iodine.
And that was why the picture of the mouse was on the, on the screen earlier because even animals which go out and hunt at night and, and potentially eat a mouse or catch prey. Could actually ingest some iodine and it could tip them back into hyperthyroidism if they were on a thyroid diet. So it's really important that if an animal is gonna be on a YD or thyroid care diet that they have absolutely no other source of nutrition, no no ability to take anything else in orally for this to work because otherwise it will fail.
And then lastly, before we wrap up this first session, we're gonna talk about canine hypothyroidism, so. Essentially everything that we just talked about in relation to metabolism, when we have too much T4, we're then gonna have the opposite of when we have too little T4. So in hypothyroidism we have decreased T4 levels, which means.
That we therefore have, you know, a decreased metabolic state. We have a lower heart rate, we have a patient which can't process, metabolise protein, carbohydrate, fats properly. They, they can't get nutrition, they don't have cell turnover, they don't have GI cell turnover, they don't have skin cell turnover, so we'll have a patient with a very, very low metabolic rate.
The causes then are split into two types, so congenital or acquired, with congenital being a little bit less common and being down to thyroid or pituitary hypoplasia, so the underdevelopment or undergrowth of the thyroid or the pituitary, meaning that the patient is not secreting as much TSH to stimulate the thyroid or the patient hasn't got a developed thyroid that's secreting levels, enough levels of T4. And then acquired, which means that patients either are suffering from a lymphocytic thyroiditis, which we'll look at in a second, or idiopathic thyroid gland atrophy, and both of those are equally as common. Lymphocytic thyroiditis then, so most dogs have a primary, which means that the level of the thyroid acquired, so not present at birth, form of the disease.
It's caused by a destructive autoimmune process, little bit like diabetes in dogs I suppose you could say, so again, one of these autoimmune processes which damage cells. And it's characterised by infiltration of the thyroid gland, by lymphocytes, macrophages, and plasma cells. So essentially those immune cells that are normally there to protect our body actually invade the tissue and they cause, granulation and scarring and, and essentially damage to the thyroid.
There's progressive replacement of thyroid tissue therefore by connective tissue. And histology examination of biopsy tissue of the thyroid would diagnose the disease, but it's not commonly done because the damage that would be done to the thyroid and parathyroid glands to do that would be sort of a lost gain if you know what I mean. So it's not something which is commonly done in these patients and instead basically what's done is that we just supplement the thyroid er hormone that is that is missing.
And then the other condition that we said that they suffer from, which is not congenital is this idiopathic thyroid gland atrophy. And it's just a degenerative process which causes the gland to atrophy. Possibly able to identify a smaller gland on ultrasound imaging in some cases, but the reasons for the changes would be unknown, so.
Again, it's essential just to replace the the hormone that is missing, but hypothyroidism caused by degenerative disease and lymphocytic disease are both equally as common and both have the same treatment, so differentiate differentiating between them is sort of less important in that way. Like with most conditions in the body, a lot of the gland has to be destroyed for clinical signs to manifest, so the body is quite good at compensating and it's the same with a lot of glands and hormones and organs in the body. So with hypothyroidism, many show few clinical signs until more than 75% of the gland is destroyed unfortunately.
The onset of the disease can be quite inconspicuous, so it can be quite a slow process and owners might not pick up on very subtle changes that happen gradually over time. And we've discussed the metabolic functions, but thyroid hormones also play a really important role in the maintenance of hair and skin turnover. So clinical signs can bluntly be divided into two sets of metabolic and dermatological for these patients.
So metabolic then, we've said that with this decrease in metabolism associated with thyroid hormone, we're gonna get lethargy, potentially bradycardia, the opposite to this hyperthyroid state. Weight gain as our metabolism slows right down. Exercise intolerance because we have, you know, the opposite of this ionotropic and prototropic cardiac effect, so, decreased ability to increase cardiac output and oxygen consumption.
A dullness, shivering or intolerance to cold because these animals might not be able to thermoregulate, and then as they progress they can have rarer signs that are more severe, which include facial paralysis, megaesophagus, laryngeal paralysis, you know, vestibular and neuropathy signs. Anywhere within the GI tract can be affected, so megaesophagus makes sense, and we'll talk about myxedema in a second, but. You know, very, very worryingly further down the line if it was to be completely undiagnosed and untreated, animals could go into mixedema coma, which is a very extreme state of weakness, coldness, dullness, and essentially the body would be shutting down.
And because thyroid hormone is involved in skin turnover, if you don't have enough of it, then we don't have enough skin cell turnover. We don't have enough, you know, change of fur, and we would have no shedding, sort of a very dry coat which is basically not turning over at the level that it normally would. And if it does, if the hair does come out, then it won't regrow, so we have some hair thinning.
We have the potential for patients to have alopecia, particularly on their flanks and thighs, which is often symmetrical and can be quite . Well associated with hypothyroidism, areas of friction, so around the collar area and the tail and the lateral extremities can have hair missing and there's this commonly associated rat's tail that hypothyroid dogs can get where they get this hair loss and thick black skin. On the tail as well, and then, as we said, coat retention can cause dullness and, and lightness due to environmental bleaching and, and low turnover of fur.
And then we get what's called this tragic facial expression because there can be an accumulation of hyaluronic acid in the dermis, so that's called myxedema. It's a non pitting edematous appearance and can make animals look quite sad like this box is shown here, so you can see thickened lips, droopy eyes and thickened skin and just a general sadness. In this patient.
And interpretation of T4 levels to diagnose hypothyroidism in patients that are clinically indicated has to be done carefully because non-thyroidal illness can occur, which frequently causes low T4 levels in dogs due to illness induced suppression rather than a thyroid gland dysfunction, so. I think it is called e thyroid sick syndrome is an expression that I've heard, and essentially, we want to make sure that patients don't have non-thyroidal illness that is causing low T4 levels when we are investigating hypothyroidism because that will obviously get confused with the patient being hypothyroid. Mild anaemia occurs in up to 44% of cases due to decreased erythropoietin production from the lack of thyroid hormone stimulation on the bone marrow, so that's something to consider as well.
And tests should include both total T4 and TSH and haematology, because as we said, previously, There's a negative feedback system which should cause TSH to be cut off when thyroid levels are high enough. So in these cases we're gonna look for a low total T4 and an increased TSH. Glucocorticoids, phenobarbital, aspirin, Carrofen, lots of medications are known to affect T4 and TSH levels, so it's really important that we make sure that patients aren't on any of those medications when we're trying to assess for hypothyroidism, and that we have a washout period of about 6 weeks.
So making sure that clients are aware that. Their pets might be off those medications for 6 weeks before we're able to actually take a blood test which could tell us if they have, hypothyroidism is really important for us as nurses to understand so that we can help support clients through what to do and, and, and discuss with them, you know, how to manage certain situations that might require those medications. And then treatment's fairly straightforward.
We're basically just replacing the thyroid hormone that the patient's missing. And as I said before with hyperthyroidism, hyperthyroidism and anti-thyroid medication, it's much nicer on the body to actually just give synthetic T4 in the form of levothyroxine, to replace the hormone that the patient is missing. It can take weeks to months to become obvious and reverse the clinical signs that we talked about earlier and especially the physical ones that we can see in the skin and the coat and the face.
So it does rely on good client communication and monitoring and for us to support throughout. It's important to know that total T4 will tell the vet more about short-term compliance, but TSH can tell the vet more about long-term compliance to medication as well, so just a few nuggets of information there which might be helpful if you're trying to help an owner that's going through, you know, a treatment, an investigation and a therapy plan with hypothyroidism. And this is what a dog looks like after we have given it some thyroid hormones.
So in the bottom right hand corner are the two pictures of her before with her tragic facial expression, and then on the left you can see her here with her recovered facial expressions and very much less tragic and sad looking. Much brighter and happier and just a different looking dog altogether, so it's quite successful and quite a nice recovery and a nice thing if you can see it. OK, so that just about wraps up part one of our two part series on endocrine nursing.
Hopefully now by the end of that session you have remembered something from your undergraduate training about anatomy and physiology of the endocrine system, but particularly we focused on sort of certain glands and the hormones that have effects on those glands. We have learned sort of more about the pancreas I suppose and the thyroid for this session, and then for the next session we are gonna focus more on the adrenals. So again, further going into those common endocrine disorders in veterinary patients, and then once we cover sort of a refresher of hyper and hypoadrenal corticism we will then move on to, Discussing diagnostic approaches for adrenal cortical patients and evaluating nursing care priorities, but we'll be focusing mostly on adrenal cortical patients as well.
So looking forward to seeing you guys there. And thank you to the webinar Yvette for having us and we will see you all at the next session.
