26 | How to actually understand the endocrine system in less than 45 minutes

PodcastEndocrine
Written By Laura Jones

If you don’t already know, the endocrine system is my absolute favourite - but that wasn’t always the case.

 

As a student nurse, I was utterly confused by the many glands and hormones, how they all linked together, and, worst of all, trying to understand a negative feedback loop!

But after years of medical nursing, I can tell you this: It is a fascinating system and responsible for some of the most common diseases we see.

Over the next few episodes, we’ll explore those diseases in detail. But before we do that, we need to understand the endocrine system and how it all works.

So, what is the endocrine system?

Well the endocrine system is a group of tissues (glands) that release hormones into circulation.

Hormones are signalling molecules that travel to a target organ or site distant from their production site. There are three types of hormones - protein and polypeptide hormones, steroid hormones, and modified amino acid hormones.

These hormones interact with receptors at their target site to exert their effects on that organ. The effects these hormones cause vary; some hormones only affect a single organ, whereas others affect multiple cells and tissues within the body. Some enhance nutrient uptake, whilst others alter cell division, for example.

Now, any tissue that secretes a substance is known as a gland. For example, pancreatic enzymes and digestive secretions, such as saliva and tears, are secreted from glands. But endocrine glands are different - they’re ductless, and instead, they secrete hormones directly into the bloodstream via capillaries that permeate the endocrine glands.

In today’s episode, I will focus on the main endocrine glands and the hormones they produce - the pituitary, thyroid, parathyroid and adrenal glands, and the endocrine pancreas.

Let’s start with the pituitary gland

The pituitary gland—or hypophysis—is the powerhouse of the endocrine system. It’s located at the base of the brain, about the size of a pea, and is connected to the hypothalamus, a portion of the brain that stimulates the pituitary gland to release certain hormones.

The pituitary gland is split into two portions: the adenohypophysis (anterior pituitary) and the neurohypophysis (posterior pituitary). Each section secretes different hormones and affects different target organs within the body.

The anterior pituitary gland

The anterior pituitary gland secretes most of our pituitary hormones from different specialised endocrine cells within it. The gland is responsible for making and releasing:

  • Adrenocorticotrophic hormone (ACTH)

  • Somatotropin (growth hormone)

  • Thyroid-stimulating hormone (TSH)

  • Follicle-stimulating hormone (FSH)

  • Luteinising hormone (LH)

  • Prolactin

The posterior pituitary gland

The posterior pituitary gland releases two primary hormones - antidiuretic hormone (ADH, also known as vasopressin) and oxytocin. 

Both hormones are synthesised in the hypothalamus but stored in and released from the posterior pituitary gland.

Let’s look at a few of those hormones in more detail

Adrenocorticotrophic hormone

ACTH affects the adrenal gland, stimulating the adrenal cortex to release cortisol. 

The hypothalamus and a negative feedback system regulate ACTH release. The hypothalamus releases CRH (corticotropin-releasing hormone), which causes the pituitary to release ACTH. 

When cortisol levels are normal, CRH and ACTH release ceases.

Thyroid-stimulating hormone

TSH works on the thyroid glands, stimulating them to secret thyroid hormones (T3 and T4). 

Like ACTH, the hypothalamus stimulates TSH release, which in turn stimulates the pituitary gland by releasing TRH (thyrotropin-releasing hormone). 

When thyroid hormone levels are within normal limits, a negative feedback system is activated. This tells the hypothalamus to stop stimulating the pituitary gland, meaning the thyroid glands do not receive any TSH.

Somatotropin

Somatotropin, or growth hormone, has many target organs, but significant ones include the liver and fat tissue. As the name suggests, it is responsible for maintaining normal growth and plays a vital role in things like glycaemic control.

We can actually see diabetes in patients with growth hormone disorders—but more on that in a future episode of this series!

Antidiuretic hormone

ADH exerts its effect on the kidneys - specifically on the distal tubule within the nephron, where it causes large volumes of water to be reabsorbed from the glomerular filtrate, concentrating the urine.

Reproductive hormones

Reproductive hormones include follicle-stimulating hormone (FSH), luteinising hormone (LH), oxytocin, and prolactin. FSH and LH trigger the release of oestrogen, prolactin stimulates lactation, and oxytocin plays a vital role in provoking parturition.

And what do we see when the pituitary gland goes wrong?

Well, the answer depends on HOW the gland has gone wrong, but pituitary disorders include hypersomatotropism (aka acromegaly), hyposomatotropism (aka pituitary dwarfism), secondary adrenal or thyroid disorders due to a lack of stimulation, and diabetes insipidus. We’ll be chatting much more about all of these throughout this podcast series.

Moving on to the thyroid gland and its hormones…

The thyroid glands are paired glands located in the ventral neck, on either side of the trachea, at the level of the 5-6th tracheal rings.

Each thyroid gland has an internal and external parathyroid gland attached to it - one at the cranial pole of the thyroid gland and one at the caudal pole.

The thyroid glands consist of thyroid epithelial cells, which secrete thyroid hormones, and parafollicular cells or C-cells, which are arranged around the epithelial cells and secrete calcitonin.

Let’s look at those thyroid hormones

T3 and T4

Epithelial cells synthesise the two thyroid hormones, thyroxine (T4) and triiodothyronine (T3), under the influence of TSH from the pituitary gland.

These hormones, formed from dietary iodine, are responsible for maintaining the body’s basal metabolic rate.

When the release of these hormones becomes excessive (hyperthyroidism) or insufficient (hypothyroidism), we’ll see a corresponding change in our patient’s metabolism.

Calcitonin

Calcitonin counteracts the effects of parathyroid hormone, reducing circulating calcium levels.

And introducing our parathyroid glands…

The parathyroids are four tiny glands (2 external and two internal parathyroid glands) located next to the thyroid glands.

Their main role is to regulate blood calcium levels within the body, which they do by releasing parathyroid hormone, aka PTH.

In a healthy patient, this is released in response to hypocalcaemia, where it works to increase blood calcium levels. However, sustained hypocalcaemia can be seen in patients with hypoparathyroidism, where insufficient PTH is released. And hypercalcaemia can be seen in patients with too much PTH, which is hyperparathyroidism.

Let’s look at parathyroid hormone for a second

The parathyroid hormone works on the bones and kidneys, converting vitamin D into its biologically active form, vitamin D3 (calcitriol). This increases calcium levels through three processes.

First, it increases calcium absorption through the GI tract. It also conserves calcium in the kidneys, preventing calcium from entering the urine. Lastly, it releases calcium from bony stores, making more calcium available in the bloodstream.

The negative feedback system is activated when calcium levels are normal, and PTH release is stopped.

What about our adrenal glands?

Now we’re on to my favourite endocrine organ - the adrenal glands.

These are paired glands located in close proximity to the kidneys (ad-renal = added to the kidneys!). They consist of an outer cortex and an inner medulla. 

The cortex is responsible for synthesising and releasing several steroid hormones - cortisol, aldosterone and androgens. 

Cortisol

Cortisol is a kind of steroid called a glucocorticoid.

It plays a crucial role in several normal body processes, including:

  • Regulating the stress response

  • Maintaining a healthy gastrointestinal tract

  • Regulating immune function

  • Regulating blood pressure

  • Increasing blood glucose levels

  • and much more.

It’s released from the adrenal cortex under the influence of ACTH—specifically, from a cortex layer known as the zona fasciculata or ZF. A negative feedback system, which shuts off ACTH release when cortisol levels are normal, maintains correct cortisol levels.

Excessive cortisol is seen in patients with Cushing’s disease, aka hyperadrenocorticism - whereas low cortisol levels are seen in patients with Addison’s disease, or hypoadrenocorticism.

Aldosterone

Aldosterone is a type of steroid hormone known as a mineralocorticoid. It’s released from a layer of the adrenal cortex known as the zona glomerulosa, or ZG, in response to the release of a hormone called renin.

Renin is released by cells in the kidney in response to reduced renal blood flow. It ultimately causes aldosterone release, increasing blood pressure and renal blood flow.

Aldosterone’s primary function is to maintain fluid and electrolyte balance. It does this by acting on the renal tubules in the kidneys to promote potassium excretion and sodium reabsorption from the glomerular filtrate. 

Because sodium and fluid are closely linked, when sodium is reabsorbed into the bloodstream, fluid retention also occurs - increasing plasma volume and, in turn, blood pressure.

It’s the loss of this hormone that’s responsible for the acute crises we see in Addison’s disease - but more on that in a future episode in this series.

What about our other adrenal hormones?

So far, we’ve only really chatted about the adrenal cortex. But what about the medulla, the central portion of the adrenal gland?

The adrenal medulla contains neuroendocrine tissue—cells not just capable of releasing hormones but also under the influence of our sympathetic nervous system, the part of our nervous system responsible for our ‘fight or flight’ response.

When this is activated, the cells in the adrenal medulla release stress hormones, including adrenaline (epinephrine), noradrenaline (norepinephrine), and a little dopamine.

We can see tumours affecting the adrenal medulla, causing sporadic release of these hormones. This can be incredibly dangerous, as life-threatening tachycardia, hypertension, and arrhythmias can result.

And then we have the pancreas

The pancreas is a bilobed organ in the cranial abdomen between the stomach and the duodenum. 

It’s a very clever organ with both exocrine and endocrine functions. 

The exocrine functions occur within pancreatic acinar cells, responsible for the formation and secretion of digestive enzymes.

The endocrine cells sit within the Islets of Langerhans. There are four types of endocrine cells: alpha, beta, delta, and PP cells. Though they do have some other functions, they’re predominantly responsible for glucose homeostasis, which is mainly achieved through the release of glucagon and insulin.

Glucagon

Glucagon is secreted from alpha cells within the Islets and increases blood glucose levels by converting stored glycogen in the liver into glucose through glycogenolysis.

It’s one of several counter-regulatory hormones released as an emergency in a hypoglycaemic patient to rapidly increase circulating glucose levels.

Insulin

Insulin is released from beta cells in response to elevated blood glucose levels. This hormone reduces blood glucose by stimulating fat, liver and muscle tissue to store glucose, reducing circulating glucose levels through a process known as gluconeogenesis.

Two other hormones/peptides secreted by cells within the pancreatic Islets are pancreatic polypeptide and somatostatin.

Somatostatin

Somatostatin is secreted from delta cells. It inhibits growth hormone, which is released from the anterior pituitary gland.

Pancreatic polypeptide

Pancreatic polypeptide is secreted from F (or PP) cells. It is responsible for maintaining pancreatic function and storing glycogen within the liver.

So, what problems do we see with the endocrine pancreas?

The most common pancreatic endocrine disease we see is diabetes mellitus, in which insulin is deficient or ineffective. However, we can also see both insulin- and glucagon-secreting tumours causing periods of hypoglycaemia or hyperglycaemia, respectively.

Diabetes is a particularly important endocrinopathy for us to consider because we see it so often—and as nurses, we have a huge role to play in the care of these patients! Because of this, we’re going to dedicate a few episodes to it—and I’ve also got a special announcement relating to this in next week’s episode, which you won’t want to miss!

We’ve touched on negative feedback a lot today - but what does it actually mean?

We’ve mentioned many different hormones, but how does our body control their levels and stop their over- or under-production?

Well, it does it via something called negative feedback. But what is this, and how does it work?

To understand how the negative feedback system works, we must first know this: our bodies and our patients’ bodies must be kept as constant as possible. Fluid balance/water concentration, glucose levels, and cortisol levels must all be controlled within a tight range. 

The body has control systems, known as negative feedback systems or negative feedback loops, to help regulate levels of different hormones and maintain homeostasis. 

It’s especially important that we understand this in one endocrine disease—hyperadrenocorticism, aka Cushing’s disease. I’ll explain why properly in our Cushing’s episode, but basically, there are two types of Cushing’s, and they affect the negative feedback system differently.

In essence, a negative feedback system is this: when the levels of a particular substance move out of the ideal range, corrective mechanisms within the body are switched on or off as needed to restore the balance.

For example, let’s look at the relationship between the thyroid and the pituitary gland.

Under instruction from the hypothalamus, the thyroid and pituitary gland work together to regulate the amount of circulating thyroid hormone (T4). Here’s what happens when T4 levels change and how the negative feedback system responds:

  1. T4 levels drop below normal.

  2. The hypothalamus detects this change. 

  3. It stimulates the pituitary gland to release TSH, which stimulates the thyroid gland to release more thyroid hormone. 

  4. It then detects that levels have returned to normal and stops telling the pituitary gland to release TSH. 

  5. Once levels drop again, the system re-activates, and the cycle repeats.

And let’s look at the relationship between the hypothalamus, pituitary gland, and adrenal gland…

You may hear this referred to as the hypothalamic-pituitary-adrenal axis or HPAA. This is how it works:

  1. The patient’s cortisol drops below normal (let’s say a stressful event has just used some, and the patient now needs more)

  2. The hypothalamus detects a drop in cortisol level

  3. It stimulates the pituitary gland (via the release of CRH) to start making and secreting ACTH

  4. The ACTH heads to the adrenal cortex and begins stimulating it, causing it to release cortisol

  5. Cortisol levels increase back to normal

  6. The hypothalamus detects this change and stops releasing CRH, shutting down the cycle and preventing excessive cortisol release.



So there you have it! Yes, the endocrine system can be complicated, but by understanding how our major endocrine glands - the pituitary, thyroid, parathyroid, adrenal and pancreas - work and what their hormones are supposed to do, we can start to understand what happens in patients with endocrine disease more easily.

And that’s precisely what we will spend the rest of this series doing! In the next episode, we’ll start to look at the pancreas and diabetes before we jump into our other endocrine disorders in more detail. By the end of this series, you’ll feel way more confident nursing endocrine patients - and I can’t wait to learn with you while you do it!

Did you enjoy this episode? If so, I’d love to hear what you thought - screenshot it and tag me on Instagram (@vetinternalmedicinenursing) so I can give you a shout-out and share it with a colleague who’d find it helpful!

Thanks for learning with me this week, and I’ll see you next time!

References and Further Reading

Laura Jones
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