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Urticaria and Angioedema

by Stephen Holt

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    00:02 All right. Next, let's move on to urticaria and angioedema.

    00:07 Urticaria, ultimately, is caused by mast cell activation in the superficial dermis.

    00:14 Mast cells, when they degranulate, release histamine, which is why it's very pruritic, and they release a variety of vasodilators.

    00:20 And that's what causes the localized swelling and these classic raised flat lesions.

    00:25 There's 2 main ways in which mast cell activation occurs.

    00:29 There's the IgE-mediated type and then the non-IgE mediated type. Let's talk about IgE first.

    00:37 So, the IgE-mediated type is essentially a type 1 immediate allergic reaction in which the patient has previously been exposed to some trigger, has developed antibodies, and those antibodies are now binding to mast cells in the skin.

    00:52 When that patient is then re-exposed to that allergen, the IgE immediately recognizes it, triggers the mast cell, and massive degranulation occurs very readily.

    01:01 The most common allergens or drugs, like beta-lactams, food allergies can do this, insect bites like from Hymenoptera, mosquitoes, etc., infections like viruses, mycoplasma, and parasites. What you'll typically see on physical exam is a very asymmetric distribution of lesions, and they are abrupt in onset, intensely pruritic -- again, due to all that histamine -- with very well demarcated, flat, erythematous papules with central pallor. Next up, we're going to talk about the non-immune mediated causes of urticaria.

    01:35 Essentially, mast cells are still involved, but IgE is not part of the equation.

    01:39 So specific medications can do this. NSAIDs, particularly, COX inhibitors, can block prostaglandin synthesis, which allows mast cells to degranulate.

    01:49 Opioids and vancomycin actually directly stimulate mast cell activation in some circumstances.

    01:54 And then ACE inhibitors are acting via inhibition of kinin metabolism.

    01:59 In addition, there are some physical conditions that can lead to urticaria to form in susceptible hosts. Certain physical stimuli, like cold, vibration, or pressure, can lead to urticaria's emergence.

    02:13 I should just add that there are some less common associated chronic conditions that can cause this. Things like urticarial vasculitis, mastocytosis, and a variety of autoimmune diseases.

    02:24 Now, in general, urticaria are self-limited.

    02:27 The lesions only last for a few hours. And while flushing and fatigue and headache are not uncommon with a simple urticarial reaction, I do want you to be on the lookout for more severe symptoms, like throat tightness, bronchospasm, nausea or vomiting.

    02:41 That may be an indication of a more severe reaction, such as, for example, angioedema. Angioedema, by definition, is localized edema of soft tissue and mucosal tissues.

    02:53 Now, it can occur in isolation, or it may occur with urticaria or potentially with anaphylaxis. It may actually be life-threatening.

    03:00 Patients experience throat tightness, hoarseness, nausea, vomiting, diarrhea, crampy abdominal pain, and you can see a good picture of it here on the right.

    03:09 Now, you might be wondering why this tends to afflict the face and the lips and the oral tissues.

    03:15 Keep in mind that those are the loosest tissues in your body.

    03:18 So while this lesion, this process may be happening in all the skin in the body, it's these loose connective tissues around the lips, the face, the tongue, the throat, and the genitalia that can cause these complications.

    03:29 The mechanism is 1 of 2 different ways.

    03:32 It can be mast cell-mediated, which means mast cell degranulation within the deeper dermis through mechanisms that are similar to urticarial lesions.

    03:40 Or it can be bradykinin-mediated, which means it's not going to require any mast cells whatsoever. Bradykinin, when it's released, increases vascular permeability. It's an inflammatory mediator just causes vasogenic edema.

    03:54 Incidentally, if there's no mast cells involved, it's going to be less itchy because you don't have mast cells degranulating histamine at the same time.

    04:01 The most common cause of bradykinin-mediated angioedema is ACE inhibitors because they directly inhibit bradykinin degradation.

    04:10 Angioedema, if it's mast cell-mediated, is going to be immediate.

    04:15 In contrast, if it's bradykinin-mediated by an ACE inhibitor, patients often report being on ACE inhibitors for months to years before developing angioedema, and it's still not clear exactly why that's the case and what precipitates the angioedema reaction.

    04:30 All right. Having talked about urticaria and angioedema, the next logical extension is to briefly mention anaphylaxis.

    04:37 Anaphylaxis is a severe type 1 hypersensitivity reaction. Patients are going to present with pruritus, urticaria, angioedema, laryngeal edema, wheezing, and nausea and vomiting. It's essentially mediated through the same pathways that urticaria and angioedema can be caused by.

    04:56 Just want to briefly mention fixed drug eruption.

    04:59 This is a situation where a patient ingests a medication, develops a specific rash, say, erythematous plaque on their left thigh.

    05:08 If they don't take that medication again for a while, and then they take it again, strangely enough, they will develop the same erythematous plaque in exactly the same location.

    05:17 That's essentially a fixed drug eruption that will happen predictably every time they're exposed to that medication.

    05:23 We've already spoken at some length about erythema multiforme, Stevens-Johnson syndrome, and toxic epidermal necrolysis.

    05:30 So let's now talk about DRESS and DHS.


    About the Lecture

    The lecture Urticaria and Angioedema by Stephen Holt is from the course Allergic and Immune-mediated Skin Disorders.


    Author of lecture Urticaria and Angioedema

     Stephen Holt

    Stephen Holt


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