Waterhouse-Friderichsen Syndrome & Addison´s Disease – Adrenal Insufficiency

by Carlo Raj, MD

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    00:01 Take a look at the picture here and we’re seeing Waterhouse-Friderichsen.

    00:03 That’s massive haemorrhage that’s taking place in the adrenals.

    00:07 What happened? That’s a fact that you had maybe an infection, meningococcemia Neisseria species or maybe perhaps DIC and DIC, what triggered this? All kinds of triggers, huh? Maybe it was acute myelogenous leukaemia type III, maybe this was a patient that had amniotic fluid emboli, maybe this was a patient that had severe sepsis.

    00:29 Whatever the case maybe, once DIC kicks in, oh my goodness, your patient looks like death.

    00:35 There is bleeding from every single orifice up and down his or her body and also internally.

    00:41 You have an increase in bleeding time PT and PTT, you have a decrease in platelet count and there might be massive haemorrhage into both of your adrenals resulting in primary adrenal insufficiency.

    00:53 Let’s take a look at the symptoms of both primary and secondary adrenal insufficiency.

    00:59 If you have complete destruction that’s taking place of your adrenal gland, then you can expect the following.

    01:06 You do not have cortisol, you do not have aldosterone and you might not be producing your adrenal androgens.

    01:13 If you don’t have aldosterone, you can expect your blood pressure to be extremely weak.

    01:18 If you don’t have aldosterone, you can expect to… you can expect the patient to not have much sodium.

    01:23 If you don’t have aldosterone, you can expect hyperkalemia and if you don’t have aldosterone, then you can expect your PH to be decreased, right? If you don’t have cortisol, adrenal insufficiency.

    01:35 Wow, you are worried about death.

    01:38 So, with all that said, weakness, weight loss, anorexia, nausea, vomiting, weakness especially maybe due to hypokalemia, there will be hypotension because there is no aldosterone, but that will be much more pronounced in primary.

    01:54 What’s the difference in primary and secondary? Primary is the adrenal gland itself being destroyed by many, many, many causes including autoimmune disease, maybe infection, maybe Waterhouse-Friderichsen, maybe iron overload and such.

    02:08 Secondary would mean that the anterior pituitary is not working properly and therefore, not releasing ACTH.

    02:16 Hyponatremia, less common in secondary, more pronounced in primary because you don’t have the aldosterone.

    02:24 Are we clear? The entire adrenal gland is being destroyed.

    02:28 There is something called acute adrenal insufficiency; in other words, it’s a crisis.

    02:36 What is the most important stress hormone again? Cortisol, so can be precipitated by severe physiologic stress such as surgery, sepsis that’s pretty severe, significant stress.

    02:50 In patients with chronic adrenal insufficiency or by rapid development of AI is what’s referred to as being our crisis.

    03:02 Adrenal haemorrhage, pituitary apoplexy may result in complete lack of cortisol being supplied to the patient because the adrenal or maybe perhaps the pituitary has lost complete function during such physiologic severe stresses.

    03:21 This is crisis… sudden death, no cortisol.

    03:25 That is how important cortisol is to you.

    03:29 Here, we have POMC, what this picture is going to show you is up in the anterior pituitary, proopiomelanocortin opio referring to your beta endorphin; melano then referring to your melanocytes stimulating hormone and you have ACTH.

    03:50 If it’s primary adrenal insufficiency such as Addison’s, what is your ACTH level? Elevated.

    03:57 What about POMC? Elevated.

    03:59 If there’s such melano, then what does your patient look like especially around the mouth region? Oral mucosa, might be hyper pigmented, how come? Because the melano, melano, melano… melanocytes stimulating hormone.

    04:13 If you had secondary adrenal insufficiency, my problem is in the pituitary gland; there’s no ACTH obviously there won’t be hyperpigmentation.

    04:23 Hyperpigmentation is my topic of the skin and what you’re noticing here is hyperpigmentation of your oral mucosa; hyperkalemia due to loss of aldosterone.

    04:40 Secondary adrenal insufficiency, where is my problem? Grouped together hypothalamus and pituitary you focus upon the pituitary; hypothalamus will be technically called your tertiary adrenal insufficiency.

    04:53 At least know two causes of adrenal insufficiency, primary or secondary.

    05:01 Causes… metastatic cancer, what is the cancer invading? The pituitary; infection, infarction, Sheehan, irradiation.

    05:15 All of these maybe then causing damage to whom? The pituitary topic secondary.

    05:20 There’s no hyperpigmentation because there isn’t enough ACTH, there’s no hyperkalemia as aldosterone is unaffected.

    05:29 That’s incredibly important.

    05:31 See, you have secondary adrenal insufficiency and you are focusing upon the ACTH.

    05:39 Why in the world is hyperkalemia not pronounced in secondary adrenal insufficiency? Because ACTH, as I’ve mentioned numerous times, plays only a minor role in aldosterone feedback.

    05:55 Your major role for aldosterone feedback would be your RAAS system.

    05:59 So, therefore, even though ACTH and it not being there might affect your aldosterone negatively, please understand that you still would have proper feedback because renin is not being affected.

    06:13 Clinically, that is absolutely critical for you to understand.

    06:19 Pathology here, if you don’t have ACTH, gone are the adrenals.

    06:24 So, now, coming back to my point.

    06:26 Yet once again, exogenous use of cortisol, what does your patient look like? Prototypical Cushing’s… moon facies and so on and so forth.

    06:38 Inside the body, what’s happening? Secondary adrenal insufficiency.

    06:42 Secondary because both of the adrenals are now undergoing atrophy.

    06:45 Fascinating! So, what do you want to do? Next step of management: once the use of prednisone clinically is done, you as a doctor have now understood that prednisone has completed the job for the patient.

    07:02 Never stop the prednisone abruptly and you make sure you emphasize that to the patient, don’t just say to-say it passively.

    07:10 You need to make sure that you actively and convincingly tell the patient, you wean the patient off the prednisone, you have to because the adrenals are atrophied or your patient’s dead.

    07:24 Do you want to be in practice? Do you see what I’m saying? Obviously, I’m being dramatic, but it’s important that you understand that.

    About the Lecture

    The lecture Waterhouse-Friderichsen Syndrome & Addison´s Disease – Adrenal Insufficiency by Carlo Raj, MD is from the course Adrenal Gland Disorders.

    Included Quiz Questions

    1. Meningococcemia
    2. Viremia
    3. Stapholococcus
    4. CMV
    5. Streptococcus
    1. Central obesity
    2. Hypotension
    3. Hyponatremia
    4. Weight loss
    5. Weakness
    1. Increased POMC leading to increased MSH
    2. Increased blood flow due to increased cortisol levels
    3. Increased POMC leading to increased ACTH
    4. Hypertension and cyanosis
    5. Increased ACTH leading to increased melanin deposition
    1. Hyperaldosteronism
    2. Low ACTH levels
    3. No hyperpigmentation of oral mucosa
    4. No hyperkalemia
    5. Disorder of hypothalamus and pituitary

    Author of lecture Waterhouse-Friderichsen Syndrome & Addison´s Disease – Adrenal Insufficiency

     Carlo Raj, MD

    Carlo Raj, MD

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    Very detailed and informative information...
    By John H. on 12. August 2017 for Waterhouse-Friderichsen Syndrome & Addison´s Disease – Adrenal Insufficiency

    This is a very clear and concise lecture about Adrenal Insufficiency.