Hi everybody and welcome back to our 2nd part of our two part series. Nursing patients with adrenal cortical disease is going to be the focus of this session. Thanks for joining me again.
So in part one we refreshed our knowledge of the anatomy and physiology of the endocrine system. We've had a look at what hormones are and what hormones are involved in maintaining homeostasis. We started to look at some of the more common endocrine disorders out of the list that we'll, we'll remind ourselves about those conditions in a second.
And then this week we're gonna move on to some other endocrine disorders and we're gonna be focusing on those patients that have got adrenal cortical disease. We're gonna be looking at some diagnostic approaches for adrenal cortical disease patients and we are gonna be evaluating some nursing care priorities and thinking about how we would nurse hyper and hypoadrenal corticistic patients. So in the last session we said that the body is like this little post office with the endocrine system being this mail delivery system.
That sends and receives these chemical messenger signals to the different organs around the body. We covered the thyroid, the pancreas and a little bit of pituitary, and this session we're going to cover the pituitary in more detail with the adrenal glands and how those organs work together. And then across both sections we'll have done the most common endocrine diseases in cats and dogs because we've previously covered hyperthyroidism, hypothyroidism and diabetes, and then in this session we're doing hyperadrenalcorticism and hypoadrenalcorticism.
So a little bit of an anatomy and physiology refresher then, the adrenal glands are named adrenal, for then er proximity to the kidneys, so additional to the renal gland. They're two glands, they sit cranial to the kidney, one on the left and one on the right. And each gland is made up of two separate hormone producing sections, so we've got the adrenal medulla and the adrenal cortex.
And the medulla and cortex have completely different functions and they do regulate different parts of the body. So the adrenal cortex then, that's the little bit around the outside of the gland that you can see there that I'm pointing to with the arrow on the diagram. That develops from glandular tissue, it responds when it's stimulated by adrenal corticotropic hormone, or ACTH that's produced in the anterior pituitary, so the pituitary produces ACTH and the adrenal cortex responds.
Hopefully when you start to see, us talk about ACTH and and how it stimulates the adrenal glands and things like that, we start to think about when we're testing and we're doing ACTH stimulation tests and things like that, and this all starts to make sense. It produces a variety of hormones that can be grouped sort of grossly into three main types. So we've got our glucocorticoid hormones, we've got our minerala corticoid hormones, and we've got our sex hormones.
Glucocorticoid and mineral corticoid hormones are called steroids or corticosteroids. And they're all structurally very similar, so they've all got these 44 carbon atom rings, which I find really interesting. So there's an example of what they look like on the screen there with their 4 carbon atom rings and there's the very common glucocorticoids that we talk about in practise, a cortisol, cortisone and corticosterone.
So those are the very common glucocorticoids that we're dealing with. They're named due to their main function, and that is to increase the levels of glucose in the blood by stimulating gluconeogenesis in the liver. So in the liver, when protein, glycogen and sometimes fat is converted to glucose through a series of chain reactions, that's known as glucoogenesis, and glucocorticoids, so glucose corticoid.
Is responsible for that. They're also really useful because they interfere with the release of inflammatory cells in the body, so they have this anti-inflammatory effect and that's why we then will give synthetic leucocorticoids as an anti-inflammatory. They're involved in the metabolism of carbohydrates in the body, so without glucocorticoids we can't correctly metabolise and use carbohydrates either.
And minerallo quarticoids then these play a completely different role, so they're responsible for metabolism and regulation of electrolytes and water balance. The most important one that we talk about is aldosterone in our patients in terms of hypoadrenalcorticism. And aldosterone targets the kidney, it causes the reabsorption of sodium ions from urine back into the bloodstream and it exchanges them for potassium and hydrogen ions.
Water's also absorbed with sodium, so aldosterone can affect water levels and we'll look a little bit more. At this in detail when we talk about our Addisonian patients later. So just for completion then, we have the cortex that we talked about for our glucocorticoid and minerala corticoid production.
But we also have a medulla in the adrenal gland, which is this inner tissue which er we're pointing at on the screen here with our arrow. And it's more sort of like nervous tissue and it's affected by the nervous system releasing and regulating adrenaline and noradrenaline, so that's what the medulla is responsible for. So let's look at how those adrenal glands work with the pituitary then.
So this is the hypothalamus pituitary adrenal cortical axis, you'll have to forgive my very sketchy drawing here. But essentially what it tries to explain is how this system works in terms of the pituitary producing ACTH and the adrenal glands responding to it. So what happens is the.
Just get my laser pointer. The hypothalamus in the brain senses a drop in cortisol levels, so the cortisol levels in the bloodstream drop below a certain value, and the hypothalamus and the pituitary together actually both sense that drop. So the hypothalamus will produce a corticotropin releasing hormone or CRH and the pituitary responds to the CRH as well as responding to the directly to the cortisol levels in the bloodstream.
And produces ACTH, which stimulates the adrenal glands to produce cortisol. The cortisol levels in the bloodstream rise, and as I'll show you in a second, then the pituitary suppresses the ACTH that's being released. So ACTH, as we said, stimulates the adrenal glands to produce cortisol.
Now what's important is that this isn't just a very steady, beautiful stream of hormone that's being produced by either gland at any point. These hormones are episodic and fluctuating, and that's sort of what makes it a little bit more difficult to interpret test results sometimes. But essentially, as I said, the levels of cortisol reach a certain point.
And then they are suppressed by the negative feedback system when the hypothalamus and pituitary levels sense that they're high enough. So they stop producing ACTH, and that suppression occurs at different time points immediately, intermediately and delayed. But essentially the adrenal glands are no longer stimulated to produce cortisol, and so the cortisol levels in the bloodstream will drop.
So what's happening in our patients then where this axis has stopped working, so our patients that have hyperadrenal corticism, most commonly will have a primary dependent hyperadrenal corticism. So what that means is it's a malfunction with the body, there's no external influences that are having an impact, and that's the most common type, it's, it's the type that at least 80% of patients will have when they have hyperadrenal corticism. Out of those that do have it, there'll be a combination of patients that have got a functioning pituitary tumour, which is the most common type to have, so about 85 to 90% of patients will have pituitary dependent hyperaddrenal corticism, or they may have a functioning adrenal, tumour as well.
So about 15% of patients that have Cushing's will have that. So what happens then is essentially with a functioning pituitary tumour, of which an adenoma is most common, you can have a carcinoma. Essentially what's happening is the tumour is autonomously kicking out ACTH.
It's not listening to the negative feedback system, it's stimulating the adrenal glands, and it, it's just not, listening to the levels of cortisol that are in the bloodstream. It's not suppressing the ACTH that's being produced in response to the levels of cortisol in the bloodstream. And so you'll have this bilateral enlarged adrenal hyperplasia potentially with this condition.
Because it's gonna stimulate both the adrenal glands at the same time, so with pituitary dependent hyperadrenal corticism, there is commonly a bilaterally enlarged adrenal hyperplasia as well. Then what you'll have potentially, like I said in those 15% of patients is a functioning adrenal tumour. And that's just a tumour that's not listening to the amount of ACTH that is or isn't being produced.
So you'll have a unilateral tumour on one of the adrenal glands, and it's just. Autonomously kicking out cortisol into the bloodstream. The ACTH by the pituitary can be suppressed, can be cut off, and it won't make any difference because the adrenal glands aren't being stimulated by that.
It's a tumour that's just kicking out cortisol itself. So that's the two types of primary dependent. And then you can have a situation where you have an iatrogenic hyperdrenal corticism where there is potential overdose of exogenous corticosteroids and we're essentially doing the work of the adrenals for them.
If we give a load of steroids chronically, what will happen is we will start, we will essentially be doing the work of the adrenal glands and we'll be creating a hyperadrenal corticism. Ourselves by giving that. There's other conditions as well, that can cause, hyper adrenal corticism as well, so there's, other reasons why you can have, patients that have hyperadrenal corticism, that aren't responsible for, aren't associated with being a primary dependent reason.
But as we said, this is, this is the most common reason, is to have a functioning pituitary tumour or an adrenal tumour. So let's have a look then at what cortisol does. So in order to be able to fully understand what a patient with too much cortisol has going on, we really need to understand what what an appropriate level of cortisol is supposed to do and.
Culturally I think now everybody is a bit worried about cortisol because it's just kind of a hot topic this past few years about it being a stress hormone and how to keep our cortisol levels down and how to maintain, you know, good cortisol levels in life. We kind of forget how amazing cortisol is and what it was designed to do. So cortisol usually is, is responsible for maintaining blood glucose levels, and it does that by increasing gluconeogenesis in the liver and counteracting the effect of insulin.
So it has an element of insulin blocking ability. It's useful because in a stressful situation we want our brain to have access to as much glucose as possible. And in order to do that, cortisol will block insulin receptors, which will mean that we can't absorb the glucose into other cells that we need around the body as much, and therefore there'll be more in the bloodstream for the brain to use, so it's very clever.
And in order to increase gluconogenesis in the liver, we need to be able to find amino acids from somewhere to be able to go to the liver and be made into glucose, in a stressful or starved state. So what cortisol does is it, contributes to protein and fat breakdown. In order to get those amino acids that can then be used by the liver to make glucose, in a normal healthy patient, also what it's useful for is inhibiting inflammatory pathways.
There are multiple very complex ways that it does that, one of the most easy and straightforward ways that I, remember that it does it is by, affecting the macrophages and stopping white cells from working as well, so when we have inflammation, we quite often have, a cascade of white cells go to an area and sort of, congest an area if you like, and that actually is what's responsible for part of the inflammation and and the pain and the swelling. so cortisol also has an inflammatory inhibition, pathway route as well, where it does many things, one of which is it affects, macrophages and how they work. And that's all very, very, very amazing, and when it's at the right level, and our endocrine systems are working properly, cortisol is really truly the most amazing hormone.
But we know that our patients that have got hyperadrenal corticism unfortunately have excessive levels of cortisol circulating in the bloodstream and chronic levels as well, so high levels for long periods of time. So when we think about what cortisol does in the body that we've just talked about, then we need to think about all of those things in excess and what that means in a hyperadrenal corticism patient. So when we think about blood glucose levels being maintained in a normal patient, then somebody with er a patient with too much cortisol is gonna have raised blood glucose levels.
They're not gonna be able to utilise them properly in all of the other cells across the body because whilst it's great that the brain has excess glucose if it needs it. The rest of the cells in the body can't actually have the glucose enter the cells and because of the insulin resistance that cortisol can cause. We've said that muscle and fat wastage that normally is useful to to break down the energy sources for amino acids, for gluconogenesis, can then actually become excessive and we get these patients that have this catabolic state, so they they present with these.
Potbellied appearances I guess is, is the classic one where the muscle is broken down, and the patient can't support the weight of their, their tummy anymore and we get this sort of dropped potbelly appearance. What normally is an anti-inflammatory response and an ability for cortisol to sort of affect inflammatory pathways, when we think about chronic long-term exposure to cortisol. It then has an impact on the immune system, so, it can turn into an immunosuppressed patient.
And we use that, don't we, we utilise that in to our benefit when we, when we want to immunosuppress a patient, we will give them synthetic cortisol in the terms in, in the, in the terms of steroids and prednisolone, is the most common one. So cortisol that's useful during periods of long-term stress, such as starvation, chronic inflammation or infection, it then begins to have a detrimental effect on the body. So as we saw in the previous slide then and for this guy here we do see these patients coming in with this skin thinning and hair loss appearance.
They may be dull, they're gonna look potentially like they've got too much stress hormone coursing through their veins, they're gonna look stressed. So panting is quite common, tachycardia, tachypnea. They do get this, this sad, dermal connective tissue atrophy.
Again, as we said, glucose can't enter the cells correctly in, in patients, so the cells aren't able to utilise the energy that they need to turn over and to reproduce and so, you get this sort of dermal connective tissue atrophy. Polyphagia and polydipsia is a direct result of the glucocorticoid centrally occurs, and we know that our patients, present very commonly in PUPD for, hypergenocorticism. We said, didn't we, about this abdominal distention, redistribution of fat to the abdomen combined with muscle, wastage will give this potbellied appearance, and they may also have liver enlargement, because the liver is becoming very, very congested because these patients are quite often trying to.
Maintain gluconeogenesis, and sort of glucose, regulate glucose balances, and so that the liver is really working hard and does get sort of, very congested with, amino acids, so you'll see liver enlargement, patients will have very voracious appetite because they can't get the energy they need, a little bit like a diabetic, they can't get the energy that they need from the glucose that's circulating. And they'll have muscle wastage and weakness, and we said that's a a direct result of metabolism of protein. They may be neurological, and hypertension can be associated, but it's a bit less common.
As the disease progresses we might have immunosuppression so severe that we'll end up with wound breakdown. Patients can have congestive heart failure, signs with that are associated with a head mass, so if it's a pituitary dependent hydrenal corticism, that is a a brain tumour essentially and so further down the line if the mass was to get larger, you could have signs associated with a sore head such as head pressing. You know, signs that are associated with brain problems such as ataxia, blindness, seizures, and things like that.
Patients can actually present with, a sort of a severe condition called pseudomyotonia where the muscles aren't able to relax and they've got this really stiff gait, sort of very interesting but not so surprising, actually, resolution of degenerative joint disease can be seen in these patients due to the, excess levels of anti-inflammatories that are circulating. Facial paralysis, SARS, hypercoagulous states, pulmonary thromboembolisms, insulin resistance, diabetic signs, all sort of more severe and less common clinical signs that are associated with prolonged and severe disease but can be, can be certainly, clinical signs that are able to present in these patients. So diagnosis then, so blood work will consist of a number of er profiles and tests.
So one of the things that's associated with having too much stress hormone is this white cell pattern which is known as a stress leucogram. So that's where er vets will look at the endogenous corticosteroid effects on the blood cells. So in a patient that's got too much cortisol, you will have a neutrophilia, and that's because of a change in the structure of neutrophils which stops them attaching to the vessel walls, so it causes what's called demarginalization, so there's more circulating, so you'll have an increased number of neutrophils in the bloodstream on a test, but what you won't have is a left shift, so, a left shift is basically an increased number of immature neutrophils in the bloodstream, and that's often caused when, The bone marrow has to release neutrophils quickly due to something like an infection, or some reason where the mature neutrophils have been consumed, and that doesn't happen with a patient with er too much cortisol.
Then you'll also get a lymphopenia, so low lymphocytes, because the cortisol essentially can cause lymphocyte cell death, decrease the rate of circulation. And sequester lymphocytes out of the bloodstream and trap them in the lymph nodes and things like that, so you'll get a lymphopenia. And then you'll also get an eosinopenia, because of the cortisol inhibiting the release of the eosinophils from bone marrow.
So as I said, that whole profile together is known as a stress leucogram, and vets will be looking for that when they're testing for hyperadrenal corticism. They may also do a biochemistry panel to sort of check what the the organs are doing and how they're functioning and how they're coping with the disease or check that there's not another reason that we've missed that this patient has too much cortisol, and that this is a sort of secondary condition rather than a primary or something like that. They'll quite often look at the liver markers because we said the liver is actually under quite a lot of stress.
So they might see an increased alk phos, they might see a high end of fasting blood glucose range because they're going to, have too much blood glucose in the, in, as we said, because of the insulin resistance, and they might see an increased cholesterol, triglycerides, and bile salts as well. They might look at a urinalysis. These patients are quite often going to have a bit of a low specific gravity, but they are able to concentrate their urine if required due to the the polyurea, polydipsia that they're going to have.
So an SG of potentially less than the 1.015. Urine retention with an overextended bladder, overdistended bladder is quite common, and as we said, muscle wastage and immunosuppression, is common in these patients, and unfortunately that can contribute to a urinary tract infection.
They may have protein urea and glucosurea. Because of that, inability for glucose to enter the cells, you're gonna have an increased level of glucose in the bloodstream and you're gonna exceed the renal threshold. So glucose is gonna, cross the renal membrane and be excreted in the urine.
Radiographs might show a liver enlargement, as we said previously, they might show this potbellied appearance sort of with the, with the fat in the abdomen, as we just said, they may show an extended bladder, and they may show adrenal enlargement or mineralization. It's not common that the adrenals are very easy to see otherwise, but potentially if you're very good at X-raying and, and, and sort of looking at X-rays and the adrenals are very big, they may be visible. It could show pulmonary metastatic disease if the adrenal tumour is a carcinoma sadly, and then more rarely it might show that the patient has got some congestive heart failure going on as well.
Then we have our more advanced imaging modalities, which are useful for visualisation of the adrenal glands or the pituitary. So ultrasound is useful for visualising the adrenal glands. CT or MRI can be used for both adrenal and pituitary imaging and also is useful for measuring the glands.
And then MRI can be very sensitive and can actually detect pituitary tumours less than 3 millimetres in size. So there are different imaging modalities that are very useful for different things. I've got this lovely image here, of an adrenal mass on this patient here, which I just wanted to show you, which is really nice.
OK, so we've talked through the types of general blood tests that patients might have when the clinicians are trying to support a diagnosis of hyperadrenal corticism such as a stress leucogram, and a biochemistry profile. But now looking at the more specific tests then that clinicians will use to support a diagnosis of hyperaddrenal corticism, let's have a chat about these, so. Blood tests that are used can include endogenous ACTH, so endogenous just means naturally occurring ACTH, and we can combine that with ultrasound, which is thought to be a good diagnostic protocol.
The idea behind that is that a patient with a pituitary tumour is going to be producing very high levels of ACTH. And a patient with an adrenal tumour is gonna hopefully have its ACTH suppressed by a healthy pituitary, so it would have a lower level of ACTH, and then if you combine that with ultrasound, then you might see some adrenal enlargement which can be a good diagnostic tool. The next test which was commonly used is the ACTH stimulation test, so that's where we essentially do the job of the pituitary for a moment and we inject synthetic adrenal corticotropic hormone.
We do expect that the adrenal glands will then produce more cortisol, which will then suppress the results, suppress the ACTH the pituitary is producing. And so we should see in a normal patient, we should see a level of suppression and sort of a low, reading, once we've injected a synthetic ACTH, a lower reading. In a patient that's got hyperadrenal corticism, the adrenal gland is already producing very high levels of ACTH.
The pituitary gland is already producing very high levels of ACTH and it's already very overstimulated and so you'll see a very exaggerated response. So then these patients will have a high pre-cortisol, and a very high post cortisol, with, a very exaggerated readings, throughout which can diagnose Cushing's, but won't tell the vet whether it's a pituitary dependent or adrenal dependent, reason. And that's kind of what the low dose dexamethasone suppression test is sometimes used for.
So for that what we're really sort of testing is the ability for the pituitary to suppress the levels of ACTH that are being produced and cut off the adrenal glands from producing cortisol. So what happens there is rather than doing the job of pituitary and injecting synthetic ACTH, what we do is we do the job of the adrenal glands and we inject synthetic cortisol in in the form of dexamethasone. So we then measure, so we measure a baseline cortisol level, we inject synthetic cortisol, and we measure the ability for the pituitary to suppress the ACTH production and cut off the ACTH, the adrenals, which will then lower the levels of cortisol in the blood.
The idea being that if at any point the pituitary can suppress, then the, the likelihood is that it is a pituitary tumour. If the pituitary cannot suppress, at any point, then it's more likely to be an adrenal tumour, because it doesn't really matter how much dexamethasone you, inject, either in a in a low dose or a high dose, you should not ever have any suppression if it's an adrenal tumour. If there is the ability for the pituitary to suppress at any point, then it could be a pituitary tumour, because some healthy pituitary tumour tissue still remains and it is able to suppress, and the fact that it hasn't just completely over-exaggerated the reading throughout indicates more that it's not an adrenal tumour.
So that's basically what happens when you do a low dose dexamethasone suppression test. With a high dose, basically what is happening is we're saying, OK, so the pituitary hasn't suppressed with a low dose, let's see if we can give it even more cortisol and stimulate the healthy tissue, in the pituitary to work, and suppress the levels of ACTH that are being produced, and cut off the adrenals from producing cortisol, so we give it even more of the of the same drug which is dexamethasone. Neither the ACTH or the low dose dexamethasone suppression tests are foolproof, interpretations are always carried out within the laboratory reference ranges that the bloods are being sent to, in the combination with the clinical signs and the other blood profiles that are happening, and potentially imaging as well.
In order to to to obtain a diagnosis. But the nice thing is that we can do these tests ourselves, so nurses can complete these tests and really contribute to the, the diagnostic pathway of these patients, which I think is something which is really important. So let's move on to something which is a little bit less taxing on the brain then after all of that blood test work.
So treatment options for these patients, we have common and less common associated treatment options. Mitatan was used quite commonly years back, it's an anti cancer medication that's used off licence and sometimes these days. Is still used as a second line or a backup if for some reason the patient isn't getting on with Trilista, but it's very much less commonly used now due to its ability to cause adrenal necrosis.
So what it does is it binds to adrenal proteins and destroys it destroys adrenal tissue. So it really breaks down that, cortex, adrenal cortex, and stops it from being able to produce cortisol. So yeah, much less commonly used now but still available off licence if needs be.
More commonly used these days now is this Trilista drug that we know, I think the brand is Varil that's commonly used, and it's a glucocorticoid synthesis blocking agent, it doesn't block mineral or corticoids, so we will still have some side effects associated with too much Aldosterone, it can cause severe side effects if it's not monitored and appropriately tailored, patients that have it, for too long can also suffer from, Adrenal problems, adrenal necrosis and things like that and adrenal atrophy, which then in turn can have more Addisonian type symptoms, so we need, we need to make sure that patients that are on this are being monitored appropriately. Side effects associated with these drugs are quite commonly similar to the side effects of the disease as well, so we just need to, to watch out and make sure we're not muddling the two up. If we have a patient that comes in with some clinical signs that we don't assume it's the disease not being appropriately controlled, that actually we look at the side effects that are associated with the medication.
So, trilista is associated with nausea, diarrhoea, and as I said, can be associated with hypoadrenal corticism. But survival times are much better than than no drug and also overall the prognosis is better than it is with miota. Some patients actually go down a more surgical option, so we can remove the pituitary in a hypovasectomy type procedure.
If we know that the patient has a pituitary that tumour that is gonna grow and it's gonna become worse and the patient's gonna become more sick, then we can and have done, Hypovasectomies on those cases, but we do have to remember then that we're removing the pituitary gland, which is responsible for the production of many hormones in the body, so we do have to supplement with those hormones for life. Then we can also do a very interesting surgery and remove the adrenal glands so that the, there, there's no gland to produce cortisol, but there's also no gland for the pituitary to work on. So we can do a unilateral adrenalectomy if it's a functioning adrenal tumour, but we would have to remove both adrenal glands if it was a pituitary tumour.
With that surgery, the caudal vena cava is, is, a risk, is a consideration. And the survival times are not as good as if we just do a hypovasectomy and remove the pituitary. So what are the nursing considerations associated with nursing a patient that has hyperadrenal corticism then, so all of the associated nursing requirements of a patient that has too much stress hormone, we know that they're gonna have polyuria, polydipsia, potentially anorexia, potentially polyphagia.
But also it's very important that we support the client with those, animals that have those clinical signs. It's very difficult to own a pet that has this disease because it becomes very taxing, managing it and having those, all those behavioural changes associated with eating and drinking too much can be quite stressful, so for me, a very big nursing requirement is to support the client of the pet with hypergenocorticism. We need to make sure that animals that are on medications have nursing considerations associated with nausea, sort of anti-emetics as required, diarrhoea management if they suffer from diarrhoea due to the effects of the either the disease or the medication.
We need to make sure that when they're in hospital with us, that we're controlling the stress levels that those patients are experiencing because they've already got a very overstimulated and very hard working stress response going on, so we need to make sure that they're they're given a quiet, calm environment during testing. When we're measuring stress hormone, we don't wanna influence the stress hormone levels by putting them in a very stressful environment. Outpatient testing is very useful for these patients because we can sort of give them an at home experience where their cortisol levels just might be that little bit lower.
But we we should remember that these patients are susceptible to infection, make sure that we barrier nurse them, and we don't put them at risk when they're in hospital if they're immunosuppressed by putting them next to a potentially infectious patient, but also by using hand hygiene and making sure that we wash our hands when we handle them as well. So another thing to consider about clients that own these animals is the amount of money that they're going to spend trying to treat an animal like this. And so nurse clinics are really crucial because treatments are often associated with negative side effects.
We need to be able to monitor it, but we also don't want to charge the client much, much. More money by regularly seeing the vet if we can help it, so trying to bring those costs down, making the the medication pathways, if needs be affordable, making sure the monitoring is there to pick up on underdosing, overdosing, and any clinical signs that that are developing and making sure that we treat the patient early and and and quickly if needs be. We need to make sure that we're handling the patient carefully and we're also teaching the client that they might have thin and sore skin and making sure they have comfortable beds, both in practise and at home.
Hard floors, rough beds, dirty beds can also contribute to infection and sores and wounds in these patients. So making sure that we do have those considerations intact is very important, and making sure that if we have to operate on these patients that we're aware of the increased risk of wound breakdown. Making sure that we have considered what electrolytes we might need to monitor, any hormone therapies or insulin sensitivities that we might then subsequently have afterwards if we remove a pituitary, we're going to have to replace lots of hormones in the body.
If we, suddenly stop the patient being insulin resistant, we're going to potentially have an increased insulin sensitivity. So things like that we need to consider if we're going to start removing glands as well. So we're gonna move on to hypoadrenal corticism because I'm aware that that was a very long and intense chat that we had about hypoadrenal corticism, but hopefully this is a little bit easier and straightforward to talk through and won't take quite as long and we can apply some of the knowledge that we've already learned to this as well.
So there's two types of hypoadrenal corticism. We have a primary immune mediated destruction of the adrenal glands. As Addison's disease, and that's probably more common, but we can also have, as we chatted a little bit about in the last few slides, this secondary cause as well, which is where adrenal gland atrophy occurs because we essentially administer chronic long-term steroids, and we stop the pituitary from producing ACTH because it suppresses it, because it can sense that there's enough cortisol in the bloodstream.
And essentially then what happens is our adrenal glands will atrophy because they're no longer needed to produce cortisol. So we can over time cause a secondary adrenal hypoadrenal corticism and then there's the other reasons of iatrogenic administration of medication that we talked about such as the overuse of adrenal cortical synthesis hormone blockers such as mystane and trilistane problems as well. So it doesn't really matter whether it's immune mediated destruction of the adrenal gland or whether it's iatrogenic problems causing adrenal gland atrophy, essentially a patient with hypoadrenal corticism can no longer produce cortisol or aldosterone, so glucocorticoids and mineral corticoids, production is lost.
We know from earlier the effects that cortisol have on the body, so it's very useful to think of the opposite of these when we consider a patient with low cortisol, so no ability to mount a stress response, no ability to regulate inflammation, reduced ability to regulate glucose. But we also need to learn about the importance of the loss of minerallo corticoid in hypoadrenocorticism, so we're gonna look at the loss of the main minerallo corticoid, which is aldosterone. Its function is to regulate electrolytes, particularly sodium and potassium, and it plays a role in the renin angiotensin system.
So in patients that have hypoadrenalcorticism, we're unable to fulfil that requirement. So the renin angiotensin system, we're going to call it the renin angiotensin aldosterone system for the purposes of this session. The adrenal glands and kidneys are two of the main pairs of organs in the body that work in a homeostatic way, as we've learned in the first half of this session.
They also work to maintain appropriate genesis, so creation and excretion of hormones, enzymes and electrolytes in a healthy patient. And between the kidneys and the adrenal glands, blood pressure adjustments and electrolyte balances are very tightly controlled and maintained. So what happens in the renin angiotensin aldosterone system is that the kidneys tend to drop in patient blood pressure.
They then cause renin, which is an enzyme to be released from the kidney, and renin's main job is the conversion of angiotensinogen to angiotensin one in the patient's plasma. Circulating angiotensin 1 is then activated, and that happens in and around the lung tissues by angiotensin converting enzymes, so we refer to it as ACE, and that then becomes angiotensin 2. Now once the adrenal glands sense angiotensin 2, they then release aldosterone from the adrenal cortex.
That's where this is important for a hypoadrenal corticistic patient, because if there is no functioning adrenal cortex, then they can't do that part of the process, so. Aldosterone then causes the retention of sodium in the renal tubules and with it water. So if sodium stays, then the water stays.
If the sodium leaves, however, then the water will leave. And during this process, potassium is excreted, vasoconstriction occurs, increasing the blood pressure, and the patient will probably become thirsty. Elevated plasma potassium can actually also in reverse trigger aldosterone release in a healthy patient to try and reduce levels as well.
So overall we can see that Aldosterone is heavily involved in the retention of sodium, the excretion of potassium in a healthy patient, and therefore if we think about a patient that doesn't have the ability to mount an adrenal response, so a patient that has adrenal cortex destruction. We're therefore going to have excessive potassium, and decreased sodium in those patients. We're also going to have potentially less renal perfusion, so we're going to have less excretion by the kidneys, of other electrolytes, and we quite often will see a hypercalcemia as well.
So clinical signs associated with Addisonian's disease can vary very much depending on the extent of the electrolyte imbalance, and so they therefore can be quite difficult for clinicians to interpret. As with many organs in the body, a lot of gland has to be destroyed before the clinical signs become apparent, and it's the same with the adrenal glands. As much as 90% can be damaged by the time the signs become apparent.
That's why you'll get some patients going into Addisonian crisis, and having not had a massive amount of warning before that that something is particularly wrong. But clinical signs basically are associated with the hyperkalemia and the hyponatremia that we just discussed, hypercalcemia, hypoglycemia because we have now got lowered hepatic leukonogenesis, so the opposite of when we have too much, cortisol, we've now got low cortisol. The absence of that stress leucogram that we talked about, the patient can't mount a stress leucogram if they don't have stress hormone.
Vomiting and diarrhoea is quite common, and abdominal pain with these electrolyte imbalances and these severe electrolyte shifts we'll quite often see, as we know, gastrointestinal signs, which will further then, progress the condition to an Addisonian crisis as we lose fluids through vomiting and diarrhoea as well. So the clinical signs are going to vary, like I said, depending on the electrolyte imbalance, but we'll have weak weakness, lethargy, hypertension, dehydration, bradycardia, inappotence, azotemia, all associated with electrolyte loss, dehydration and severe water, crossing the renal threshold, being taken out with sodium, and huge volume loss and dehydration. Depending on when you see a patient will depend on if they're tachycardic or bradycardic, but certainly patients will feel really unwell and if they're not vomiting and having diarrhoea then they may be inappotent.
So when does it shift then into Adetonian crisis, so patients that are severely electrolyte imbalanced then also potentially have this hypovolemia that's compounding everything because they're actually vomiting and having diarrhoea and losing water. They then present collapsed. So that is known as Addisonian crisis, they're extremely dehydrated, they've got low glucose because they can't er utilise correctly the, the mechanism of gluconogenesis in the liver.
They've got high potassium because they can't excrete it, they've got low pressure, low blood pressure and low circulating volume. It's a huge emergency, and fluids and electrolytes have to be corrected er corrected and relatively quickly or the patient may die. This can be really scary for clients, and I think that is one of the things that afterwards we should be really supporting them with because they're going to be emotionally scarred from this, and they're gonna be really worried about their patient once they've, they've gone home if they manage to get their patient home.
Hypoglycemia can also contribute to collapse, so electrolyte analysis and correction. With intravenous fluids and a sodium rich fluid, but also potentially a dextrose infusion can be the three quickest ways that we can save these patients. So, definitely checking blood glucose and making sure that they're not hypoglycemic as well, needs to happen.
So our diagnostics for these patients then are a little bit more straightforward to understand I feel, so we're looking for those electrolyte abnormalities, hyperkalemia and hyponatremia, associated with with that abnormal, excretion and reabsorption across the renal membrane. We're looking for those electrolyte abnormalities associated with extreme hypovolemia, loss of water, loss of electrolytes through vomiting and diarrhoea. We're also looking for the glucose, levels and monitoring that hypoglycemia we talked about.
We're gonna check the kidneys potentially and see if we've got elevated urine creatinine due to those altered perfusion markers. We are going to potentially do an ECG and see if we've got any associated signs of hyperkalemia in these patients, and then quite often the test of choice for these guys will be an ACTH stimulation test as well. So the ACTH stimulation test then are fairly straightforward, we're basically going to do the job of the pituitary, we're going to stimulate our patient's adrenal glands to produce cortisol by injecting synthetic ACTH and we're hoping that we're gonna see an increased level of cortisol being produced.
Obviously in a patient that doesn't have an ability to produce cortisol because the adrenal cortex is atrophied or destroyed through immune mediated disease, we're not going to be able to see that. Stimulation test be a positive test, so they're gonna flatline, they're gonna have a pre and post that's very similar to each other, and they're not gonna have an ability to, to produce cortisol from the adrenal glands. So we said didn't we, that fluid therapy is very important in these patients, they're hypovolemic, they're very dehydrated, they are collapsed due to lack of circulating volume.
They are gonna be hypoglycemic so we might often give glucose, we are gonna potentially be giving them some er electrolyte balancing adjustments, we are going to be feeding throughout, so I think that is something which is often forgotten in these patients. They do have, the ability to have necrosing GI tracts due to the fact that the blood has been diverted away to their main organs because of the shock that they're experiencing. So we do need to make sure that we maintain, a working GI tract.
So even though they are nauseous or potentially vomiting, we do need to try and manage that nausea and try and get them, them, eating something to help them recover. We need early onset nutrition, we need calories going in, and we need to make sure that we're supporting them to be able to heal. Skincare, we need to make sure that we're aware that these patients may have scaling, urinary faecal scaling, they're gonna potentially be recumbent, they're gonna have diarrhoea dripping, so making sure that we have good skincare protocols is really important as well.
And then we're obviously gonna be responsible for trying to medicate the, the, the patient in order to correct the adrenal cortex, deficit that's going on, so we need to be administering minerallo corticoids and glucocorticoids, in the forms of, both the medications that were given in hospital but then longer term transferring them onto orals as well. OK, so what are those medications then that we're talking about? So hydrocortisone is often used, it has equal glucocorticoid and minerallocorticoid action.
It can be given intravenously. It's usually the drug of choice for managing a patient in adrenal crisis, but it can be used orally to manage patients chronically as well. It has less potent glucocorticoid efficacy than both prednisolone and dexamethasone.
Dexamethasone on its own is not a desirable treatment in an adrenal crisis because there's no minerallo corticoid included, so it has very low mineralo corticoid efficacy. So, it's really only a long acting glucocorticoid and really for these patients we've got to be administering minerallocorticoids. Long term then we'd be giving DOCP or desoxycorticosterumpiolate.
It's licenced for HypoA as a mineralla corticoid, so it's administered subcut, it can be given in crisis, but it's often used for long term treatment. As it's licenced as a minerallo corticoid, clinicians will often give a glucocorticoid alongside it. We have seen some patients present to us with too much glucocorticoid activity when they're on this drug, so we do need to be careful, because it's manufactured as having no glucocorticoid activity.
But sometimes supplementary glucocorticoids can be too much. It can cause profound hypokalemia, and we we need to be careful that we're going to tailor this dose correctly because patients do sometimes present to the practise with iatrogenic hyperalsteroinism following treatment with this drug so we need to be careful you can't. Can't tailor the dose once it's administered.
Nurse clinics really do come into play here, making sure that we're monitoring patients for side effects, polyrhea, polydipsia, you know, unwanted side effects of this, of this drug being, looking like it's being given too much. Fludrocortisone then is an aldosterone analogue, meaning that it just mimics its function. It increases potassium excretion and decreases sodium excretion, and it also has some semi-glucocorticoid traits.
It was once used for the chronic management of patients with hypoadrenalcorticism. But not an adrenal crisis as it can only be given orally. The dose can be adjusted very easily.
It's very, it's, it's less commonly used now. I think for a long, long time there was problems, sourcing it, and I think people have just moved on to, DOCP now, so it's just much less commonly used. Prednisolone is often used to replace the glucocorticoid element if it's lacking, used for some but not all patients for long term treatment because again it depends on, The levels of glucocorticoid activity that they have, how much of the adrenal cortex that's producing glucocorticoid is damaged, some patients require prednisolone, but some don't, depending on what drug they're on, some of them have got some sufficient glucocorticoid activity in them so they don't need surplus, prednisolone as well.
We can induce iatrogenic hyperadrenal corticism if we give too much glucocorticoid. Hopefully everybody's, understanding of that and how that could happen is very much solidified at this point of the talk. So we touched a little bit on some of the nursing considerations when we looked at treatment, but there is a little bit of overlap.
It's gonna depend on the range of clinical signs that the patient's presenting with and that's going to depend on the level of electrolyte abnormalities that are happening, whether they have gastrointestinal disease. And signs associated with vomiting, diarrhoea, skin's gold. It's potentially going to need some intervention from us from barrier sort of proofing the skin.
Grooming, trimming away anything that's really, really soiled, giving them a good wash, offering TLC offering support to the client with a patient that's had this for a while, and helping them to support the animal at home if they've got any GI signs when they're discharged. We're going to be administering fluid therapy as we said and we're going to be trying to balance those electrolytes as needed and we're going to be monitoring bloods, using blood samples to monitor electrolytes and glucose if we have that in the practise and some practises will use the resolution of clinical signs as a way of monitoring because they don't have the ability to monitor electrolytes. We're gonna be administering medications both in practise and then teaching and guiding the owners how to do that correctly at home.
And we're gonna be making sure in practise the patient has got lots of water and educating the client as well as as to why that is very important as well. Blood pressure monitoring is going to be something which is useful because it's going to give us an idea of how well controlled the disease is, the ability for that Rein angiotensin aldosterone system to work, and the ability for the patient to regulate their blood pressure. We're going to be able to also just think about how hypovolemic a patient may be if we're monitoring blood pressure.
We're going to use assisted feeding to make sure that patients are getting the right nutrition. We chatted earlier about it, but essentially it's very important that these patients are given support to, to eat correctly and, recover correctly. Monitoring after discharge is very, very, very crucial, so making sure that, nurse clinics are in place to support the client and to monitor the patient and make sure that they, are carefully controlled on their medications going forward and that we're not under dosing or overdosing.
But really educating the client on what to look out for after treatment's going to be important because as I said at the start. Helping with fears following crisis is a huge one because owners are going to be very sensitive to what would have normally been a, a an off day. Maybe it's a hot day, maybe the animal's just a bit sleepier than normal, but they're gonna be thinking that it's going back into crisis, so, really requiring support for that.
Quality of life logs and healthcare logs are very useful for these patients and helping them to, give the client some some control over the disease and helping them to feel like they're doing something useful for their animal is often actually very, very, useful. And with all these conditions really endocrine conditions, but actually with any veterinary condition we should be thinking about holistic care. So dealing with or treating the whole of something and not just part of it, and that is something which I think nurses are very well placed to do, making sure that we think about not only the disease process but also the mental state of the animal and the physical state of that animal as well.
Just quickly before we finish up then, what do I mean when I say a mental state of an animal, and that is the, the things that a patient goes through when they come in to see us, and that is the fact that they're dealing with strangers, the fact that they're in an alien environment, you know, that fear. Of the, of not knowing where they are, who they're dealing with, everything's changed, their diet's changed, you know, their sleep pattern has changed, obviously cats and dogs have different mental states and different triggers, so we shouldn't really associate the fears that those, those species have with the same things, we should be differentiating between. Between those two, we also need to make sure that we're aware that not only are cats and dogs not to be mixed, but actually sometimes cats and cats, dogs and dogs, making sure that we, we understand the differences in, in adjustments.
That can be made to improve mental states of patients that are in with us. Patients have separation anxiety, so many animals come in and they're just so stressed out already. Just making sure that holistically we we think of these things and we address them, especially in patients that have got problems with stress hormones.
And then the last bit of holistic nursing which I like to think about are the other comorbidities that might occur and things that we might not always think of with these patients that come in. You know, have they got vision problems, you know, cataracts, we talked about polyurea, so have they got urine scold? You know, are patients self traumatising while they're in hospital, you know, thinking about them in certain kennels if they're at risk of separation anxiety, are they more at risk of nose rubs and damaged teeth?
Older patients, arthritic patients, and all of the comorbidities that come into play when we, when we think of a patient with endocrine disease, and the treatments that go hand in hand with those diseases as well. So lots and lots of things to think about, not just the disease process, for patients that have got endocrine disease, but actually that the picture as a whole is really, really useful for nurses to think about. And that's it.
So thank you everyone for joining us. Thank you to the webinar vet for having me and hopefully everyone has a little bit more of an idea of the ins and outs of endocrine nursing from this two part series. There was a lot to cram in and we haven't been able to cover everything in loads of detail, so some things have been, have been a bit superficial, but I think that overall, we've covered most things in some detail, so.
Thank you everyone again for joining me and have a great summer. What's left of it.
