June 16, 2025 • 18 mins
⚕️ FREE MSRA PODCAST – Urticaria (Hives)
🎧 A high-yield breakdown of this itchy, wheal-forming skin condition – crucial for exams and everyday clinical practice.
🧠 Key Learning Points
📌 Definition
• Urticaria (hives) is a transient, pruritic skin eruption characterised by raised, red or pale wheals that resolve within 24 hours.
• Angioedema may accompany it and involves deeper skin swelling.
📌 Causes & Risk Factors
• Allergic triggers – food, medications, insect stings
• Non-allergic – cold, heat, pressure, sunlight, vibration, stress
• Infections (especially viral), autoimmune diseases (e.g. thyroid)
• Chronic idiopathic urticaria – no identifiable cause
💡 Mnemonic: "PHYSICAL" – Pressure, Heat, Infection, Cold, Idiopathic, Autoimmune, Latex/drugs
📌 Pathophysiology
• Mast cell degranulation → histamine release
• Histamine → vasodilation + increased capillary permeability
• Results in fluid leakage → wheals + intense itching
• Angioedema = same process, but deeper tissues affected
📌 Symptoms
• Sudden onset of raised, itchy wheals (pink/red) with pale centres
• Lesions last <24 hours and move around
• Angioedema: deeper swelling of lips, eyelids, genitals
• Chronic urticaria: symptoms ≥6 weeks
📌 Differential Diagnosis
• Urticarial vasculitis (painful, persistent >24h, bruising)
• Dermatitis herpetiformis (coeliac-related itchy blisters)
• Eczema (dry, scaly, fixed)
• Bullous pemphigoid
• Polymorphic eruption of pregnancy
• Mastocytosis (urticaria pigmentosa)
📌 Diagnosis
• Primarily clinical – based on transient wheals + history
• Investigations guided by clinical suspicion
• Skin prick or IgE tests for suspected allergy
• Challenge tests for inducible types (e.g. ice for cold urticaria)
• Biopsy only if urticarial vasculitis suspected
📌 Management
• Identify and avoid triggers (physical, food, drugs, etc.)
• First-line: non-sedating H1 antihistamines (e.g. cetirizine, loratadine)
• Increase dose up to 4x for chronic urticaria if needed
• Short course of oral steroids for acute severe flares
• Second-line: montelukast, omalizumab (anti-IgE), or immunosuppressants in refractory cases
• Educate on avoidance of exacerbating factors: stress, alcohol, NSAIDs
📌 Complications
• Angioedema (esp. lips, eyelids, airway)
• Anaphylaxis in allergic urticaria – medical emergency
• Chronic symptoms → sleep disturbance, anxiety, depression
📌 Prognosis
• Acute urticaria usually self-limiting (resolves in days)
• Chronic urticaria: ~50% resolve within 3–5 years
• Persistent symptoms in ~20% after 10 years
• Poorer prognosis if associated with angioedema or autoimmune markers (e.g. antithyroid antibodies)
📎 More MSRA Resources for Urticaria
📝 Revision Notes: https://www.passthemsra.com/topic/urticaria-revision-notes/
🧠 Flashcards: https://www.passthemsra.com/topic/urticaria-flashcards/
💬 Accordion Q&A Notes: https://www.passthemsra.com/topic/urticaria-accordion-qa-notes/
🚀 Rapid Quiz: https://www.passthemsra.com/topic/urticaria-rapid-quiz/
🎓 Full Course: https://www.passthemsra.com/courses/dermatology-for-the-msra/
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Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
(00:00):
Welcome to the deep dive. Today we're jumping into a
really common condition, something you'll definitely see
Urticaria. That's right, hives.
Most people know it as hives. Exactly.
And it's crucial for things likethe MSRA exam, but also just
for, you know, everyday practise, we're going to pull
out the key high yield stuff. Yeah, the aim is to give you
that solid framework, what it is, why it happens and what you
(00:21):
actually do about it. Make it stick.
OK, let's start right at the beginning then.
What is Urticaria, clinically speaking?
Well, fundamentally it's a skin thing.
You get this sudden onset of raised itchy areas on the skin.
Wheels we call wheels, right? And the crucial bit?
They're transient. They appear, they itch, and then
(00:42):
they, well, they disappear from one spot usually within hours,
certainly less than 24 hours typically.
Transient. OK.
And what do they look like, these wheels?
You're generally looking for itchy bumps, papules, or maybe
larger patches. Plaques, often pale or white in
the middle and surrounded by redness.
That's the erythematous flare. Size and shape can vary quite a
(01:03):
lot though. Yeah, OK.
And angioedema often comes up alongside urticaria.
How does that fit? Up.
Yeah, they often go hand in hand.
Urticaria, the wheels, that superficial skin swelling.
Angioedema is deeper, deeper swelling.
Exactly. Deeper layers of the skin.
Sometimes, because membranes too, like lips or eyelids, it
might feel more tight or even a bit painful, rather than just
(01:25):
intense, intensely itchy like the wheels.
You can get both together, or sometimes just one or the other.
Got it. So wheel superficial angioedema
deeper and I remember there's a classification based on how long
it lasts. Yes, very simple.
Acute urticaria is anything lessthan six weeks, OK.
And chronic urticaria is when ithangs around for six weeks or
more. That time scale is really the
(01:46):
key split. Six weeks.
Got it. So what's actually going on
under the skin? What's the the aetiology the
'cause? Right, the core mechanism is all
about about mass cells in the skin.
They get activated immune cells.Right, yes, and when they get
triggered, they release a whole load of chemicals.
The big one everyone knows is histamine.
Histamine, hence antihistamines being the go to treatment
(02:07):
precisely so histamine and otherinflammatory stuff get released
and they affect the tiny blood vessels nearby the capillaries.
They make them leaky. Leaky capillaries and that
causes the swelling. You got it.
Fluid leaks out from the blood vessels into the skin tissue
causing that raised area of the wheel, and the histamine
(02:28):
directly hits the nerve endings,which is why it's so incredibly
itchy. OK mast cells pop, release
histamine, vessels leak, skin puffs up and itches like mad.
What makes the mast cells pop inthe 1st place?
What are the triggers? The list is pretty long.
You've got your classic allergens, certain flights,
maybe insect stings, some medications.
Right, the allergic stuff. But interestingly, it's often
(02:50):
not allergic. Physical factors are really
common triggers like what thingslike pressure on the skin, but
from tight clothing or sitting, cold, heat, sunlight, even
vibration or exercise can trigger in some people.
Infections are another big one. Viral infections, sometimes
bacterial stress, definitely a factor, and sometimes there's an
underlying autoimmune process going on.
(03:11):
That's a massive range. It is and a really important
point. Especially we talked about
chronic urticaria. Often we actually can't find a
specific trigger, it just seems to happen idiopathic or
spontaneous. Right, which must be incredibly
frustrating for patients, Absolutely.
So are some people more likely to get this?
Any specific risk factors we should know?
(03:33):
Yeah, there are a few things. Having a history of other
allergic conditions, what we call atopy.
So eczema, asthma, hay fever that makes you more prone?
OK, the etopic link. A family history of urticaria or
other allergies also increases risk and certain underlying
medical conditions, particularlyautoimmune diseases.
Thyroid disorders are quite commonly linked, for example.
(03:54):
Right, so a history of allergiesor autoimmunity flags higher
risk. Let's just quickly revisit the
how the pathophysiology mast cells histamine leaky vessels.
Yeah. So just to nail that down,
histamine and the other chemicals cause vasodilation.
The blood vessels widen and crucially, they become more
permeable. Permeable.
Leaky. Exactly like tiny garden hoses
(04:15):
suddenly springing leaks, fluid seeps out into the surrounding
tissue. That fluid collection is the
wheel, and it happens fast and usually resolves fast too as the
histamine gets broken down. Great analogy of the leaky
hoses. Is the basic mechanism the same
if it's, say, a peanut allergy versus being triggered by cold?
Well, the end result is the same.
The mast cell releases its contents.
(04:36):
You get the leaky vessels, the wheel, the itch.
The difference is how the mast cell gets that initial signal.
Allergic urticaria typically involves the immune system's Ige
antibodies recognising the allergen and telling the mast
cell to degranulate. But non allergic triggers like
cold or pressure, they seem to activate the mast cell through
different pathways, ones that don't necessarily involve Ige.
(04:59):
Different roads leading to the same mast cell activation makes
sense now. Differential diagnosis super
important. Someone comes in itchy with
raised bits. What else must be on your radar?
Well, absolutely vital because things can look similar.
Obviously IG edoema is on there.As we said, it can happen alone,
but think about dermatitis or pettiformis.
That's the coiliac related one, right?
Blisters, exactly. Intensely itchy little blisters,
(05:20):
often on elbows, knees, buttocks.
Then there's pemphagoid, anotherblistering condition, usually in
older people. Iris syphilis.
That's a bacterial infection. Usually red, hot, swollen, well
defined edge, often with fever. Doesn't tend to come and go like
Urticaria. Right, infection looks
different. What else?
Eczema can be itchy and red, of course, but the skin changes are
usually drier, maybe scaly, and they stick around the same
(05:43):
place. They're not transient like
wheels or to carry a pigmentosa.That's actually a type of
mastocytosis where you have too many mast cells.
Looks like brownish spots that turn into wheels if you rub
them. Chronic pruritus is just the
medical term for long term itching without the specific
rash of urticaria. Just.
Itching. Yeah, and polymorphic eruption
of pregnancy. PEEP or PUPPP as it used to be
(06:05):
called. Very itchy rash usually starts
in stretch marks specific to pregnancy.
Definitely one to remember for pregnant patients for sure.
And the last one, which we really need to highlight is
urticarial vasculitis. Right, you mentioned this.
How is it different and why is it so important to spot?
OK, so standard urticaria is leaky vessels.
Urticarial vasculitis is inflamed blood vessels.
(06:28):
The vessel walls themselves are inflamed.
Inflammation, not just leakiness.
Exactly. And that changes things.
The lesions in vasculitis often feel more painful or burning
rather than just inchy. They might feel a bit bruised
and critically, they last longer, usually more than 24
hours. Somebody's days.
They might even leave a faint bruise like mark or pigmentation
(06:48):
behind when they finally fade. So pain persistence over 24
hours, maybe bruising Clues for vasculitis?
And why is spotting it so crucial?
Because it's a sign of actual blood vessel inflammation, it
can be linked to underlying systemic problems, connective
tissue diseases, other autoimmune conditions, sometimes
infections, or even medications.It needs a different workup.
(07:11):
You almost always need a skin biopsy to confirm it, which you
wouldn't routinely do for simpleurticaria.
OK, that's a really key distinction.
Urticaria, itchy, transient, leaky vasculitis, painful,
persistent, inflamed, needs biopsy.
Got it. How common is plain old
urticaria epidemiology? It's very common here in the UK
(07:31):
and globally. Lifetime prevalence, The chance
of getting it at least once is thought to be around 20%.
Wow, one in five people. That's huge.
Yeah. Is that mostly the short lived
type? Yes, that 20% is mainly acute
urticaria. Chronic urticaria lasting over
six weeks is much less common, maybe around 2-3 percent
lifetime prevalence, so most episodes are brief.
OK. Acute is common, chronic is less
(07:52):
so any particular groups affected more?
Acute tends to be seen more in kids, adolescents and women
particularly. Those are the atopic background,
the eczema, asthma crowd. Chronic urticaria is a bit more
common in adults, generally OK. Thinking about seeing a patient
again, What are the absolute must know clinical features?
The core things. Two things raised itchy, pink or
(08:14):
red raised skin lesions that arepuritic, meaning itchy.
Raised and itchy? Yep.
Remember they vary in size and shape, might have that pale
centre and they disappear from one spot within 24 hours.
That transience is key. Can be anywhere on the body.
May or may not have associated angioedema.
And we talked about the clinicalsubtypes, particularly for
chromic. Right.
So acute often has no obvious cause found, but think triggers
(08:39):
allergies, infections, physical stimuli.
For chronic lasting over six weeks, you've got chronic
spontaneous urticaria. That's the one with no clear
external. Trigger exactly those stress or
underlying low grade infections might play a part than
autoimmune urticaria linked to other autoimmune conditions
where the body's own antibodies trigger the mast cells.
(09:00):
OK an inducible urticaria. This is where specific physical
things reliably bring on the hives.
Right, like the examples you give cold pressure.
Yeah, delayed pressure urticaria, cold urticaria, solar
urticaria from the sun, heat urticaria, demographism, the
skin writing one. These are all inducible types.
The history points you strongly towards them.
So if someone says every time I carry heavy shopping bags my
(09:22):
hands swell and where the handles were, you'd think.
Delayed pressure urticaria. Exactly.
History is everything for the inducible types.
And again, just to keep it in mind, Urticaria vasculitis looks
like urticaria, but remember those differences.
Pain last 24 hours, maybe bruising needs that biopsy
confirmation. Got it.
History. History.
History. So how do we actually diagnose
(09:45):
this? Do we need loads of tests?
What investigations? OK, key.
Point number one for investigations, diagnosis is
primarily clinical. Based on the story and what you
see. Exactly, history and examination
are paramount. You don't usually need a battery
of tests for straightforward acute urticaria.
So no routine bloods for everyone.
Generally no. Investigations are guided by the
(10:06):
history and clinical picture. You tailor them.
For example, if the story suggests an infection might be
the trigger, then yeah, maybe a full blood count.
Check inflammatory markers like ESR or CRP?
OK. Liver function tests?
Maybe if there are other signs suggesting systemic illness?
What about finding a specific trigger like the physical ones?
If you suspect an inducible type, you might do specific
(10:28):
challenge tests in clinic, like carefully applying an ice cube
to test for cold urticaria or controlled pressure from
pressure urticaria. Dermographism is easy to test,
just gently stroke the skin and see if a wheel forms.
The skin writing test. Simple.
Yep, if you suspect a true allergy, especially in acute
severe cases, then allergy testing might be indicated.
(10:50):
Skin prick tests or specific Igeblood tests for suspected foods
or venoms. For instance, patch testing
might be used for suspected contact triggers.
And if you're thinking autoimmune?
Then testing for things like thyroid auto antibodies could be
relevant, especially in chronic spontaneous urticaria.
Given the known link, sometimes the best test is simply stopping
(11:11):
a suspected medication or avoiding A suspected food
trigger and seeing if things improve.
Right, a therapeutic trial. What about things like H pylori
testing or urine tests? When did they come in?
H pylori testing is sometimes considered for chronic
spontaneous urticaria, particularly if there are
digestive symptoms, as eradicating it might help a
small subset of people. A urine dipstick might be done
(11:33):
if you're worried about kidney involvement, maybe hinting at a
systemic cause. Or again, urticariovasculitis,
which can sometimes affect otherorgans.
And the skin biopsy? Reserved almost exclusively for
when you suspect urticariovasculitis to look for
that blood vessel inflammation under the microscope.
So investigate smartly, based onsuspicion.
Don't just order everything makes sense.
(11:55):
Let's talk management. What do we actually do?
First step, if you can identify a trigger is obviously
avoidance. Seems simle but crucial.
Avoid the trigger. Yeah, and atient education is
key advise about potential nonspecific worsening factors.
Things like getting too hot, stress, alcohol, caffeine.
Sometimes NS is like ibuprofen, can make it worse even if
(12:16):
they're not the primary cause. OK, general advice.
What about for the itching itself?
Symptomatic relief. You can use topical things like
calamine lotion or creams containing menthol for cooling
effect. Simple but can help.
But the mainstay, the core medical treatment, is
antihistamines. The H1 blockers.
Yes, specifically the non sedating or low sedating H1
(12:38):
antihistamines. Think cetirizine, loratadine,
fexofenadine. They block histamines effects
reducing the itch in the wheels.That's first line.
And what if a standard dose, say10 milligrammes cetirizine isn't
cutting it? This is really important for
chronic urticaria management guidelines like NICE here in the
UK recommend increasing the doseof the non sedating H1
(13:00):
antihistamine. Increase the dose, How much?
You can go up to four times the standard licence dose, so for
example up to 40 milligrammes ofcetirizine or loratadine per
day. This often gets control when
standard doses fail. OK so push the first line drug
dose up before adding something else.
Good tip. What about really bad flare ups?
Acute severe hives. For those situations, a short
(13:21):
course of oral steroids like Prednisolone can give rapid
relief, usually just for a few days, maybe a week.
Quick fix? Yeah, a rescue course, but you
want to avoid long term steroid use because of all the side
effects. Absolutely.
So what happens if someone has chronic urticaria, they're on
four times the normal antihistamine dose and it's
still not controlled? What are the second line
options? Right, this is usually moving
(13:43):
into specialist territory or at least discussion with a
specialist. Options might include adding in
an anti leukotriene drug like model Lucast or move into
biologic therapy with omolizumab.
That's an injection an anti Ige antibody.
Quite effective for many with difficult chronic spontaneous
urticaria. Molizumab.
And for really tough refractory cases, immunosuppressants like
(14:06):
sicklosporin or sometimes otherslike mycophenolate or tacrolimus
might be considered, but these need careful monitoring and
specialist management so. Let's do a quick scenario.
Patient chronic hives, daily disruption.
Tried cetirizine 10 milligrammesand 20, then 40 milligrammes
daily. Still bad?
What's likely the next step? So after maxing out the non
(14:26):
sedating antihistamine dose likethat, the next typical step
often view a referral would be to consider adding omalizumab or
possibly cyclosporine. Clear pathway?
When else should you definitely refer?
OK, referral triggers, diagnosisis uncertain, symptoms aren't
controlled Despite that antihistamine dose escalation.
If they need continuous antihistamines for more than six
weeks and primary care feels stuck, definitely.
(14:49):
If you suspect urticariovasculitis, they need
that confirmation makes sense and urgent hospital admission.
Of course, if acute urticaria israpidly worsening, especially if
there's angioedema involving thethroat or tongue, or any signs
of anaphylaxis. Fairway, compromise.
Emergency. Absolutely.
Also severe acute urticaria where you strongly suspect a
(15:10):
food or latex allergy needs urgent assessment because of
that anaphylaxis risk. And sometimes really challenging
Inducible urticaria is like severe solar or cold urticaria
might need specialist input for management strategies.
OK, so identify triggers and histamines first, escalate dose
steroids for flares, then specialist options and know when
(15:31):
to refer or admit urgently. What's the long term outlook?
The prognosis? Depends hugely on acute versus
chronic. For acute urticaria, prognosis
is generally excellent. It's usually self limiting,
resolves in days or weeks, responds well to treatment.
Good news for most people then. What about the chronic form?
Chronic Urticaria. It's more persistent, more
(15:53):
unpredictable. The good news is about half of
people find their symptoms resolved within about three to
five years. OK, half get better.
Eventually a significant minority, maybe around 20%, can
still have symptoms even a decade later.
It's going to be a really long term burden for some.
Wow, a decade? Are there clues about who might
have it longer? Yes.
Factors that suggest a potentially poorer prognosis for
(16:16):
chronic spontaneous urticaria include having more severe
symptoms to start with, having angioedema alongside the wheels
and interestingly testing positive for those anti thyroid
antibodies we mentioned earlier.The autoimmune link again.
Finally, any major complicationsto worry about?
Serious physical complications are pretty rare with urticaria
itself, unless it's part of anaphylaxis.
(16:37):
But the main complication, especially with chronic
urticaria, is the impact on quality of life.
Which sounds significant. Hugely constant in the
unpredictability. The appearance changes with
angioedema. It can lead to really
significant sleep problems, insomnia.
I can imagine. And psychological distress,
anxiety, even depression are unfortunately common in people
living with severe chronic urticaria.
(16:58):
Makes total sense. Anything else?
Just to reiterate, while anaphylaxis is rare from chronic
spontaneous urticaria itself, it's always a potential risk if
the urticaria is an early sign of a severe acute allergic
reaction to something specific like a food, drug or sting.
So vigilance for systemic symptoms is always important in
(17:18):
acute onset. Right.
Always keep anaphylaxis in mind with acute hives.
OK? That covers a huge amount from
the basic definition and the leaky capillaries through
friggers, differentials like vasculitis, the investigations,
the step management, prognosis and impact.
It really shows how understanding that basic pathway
mast cell histamine leaky vessels unlocks, why it looks
(17:40):
the way it does, why it itches, and why antihistamines are the
first step in treatment. And remembering those key
differences like the transience versus persistence for
vasculitis and knowing the management pathway, especially
that antihistamine dose escalation.
It might be common, but getting the diagnosis and management
right is crucial. Absolutely.
It's about having that structured approach when you
encounter it. That was a fantastic deep dive
(18:02):
into your urticaria. Really high yield stuff.
Agreed, hopefully that sets you up well, whether it's for exams
or for seeing patients. For more free MSRA revision
resources, visit freem-sra.com and for the full Premium
Revision Toolkit, head to pass the m-sra.com.
Welcome to the deep dive. Today we're jumping into a
really common condition, something you'll definitely see
Urticaria. That's right, hives.
Most people know it as hives. Exactly.
And it's crucial for things likethe MSRA exam, but also just
for, you know, everyday practise, we're going to pull
out the key high yield stuff. Yeah, the aim is to give you
that solid framework, what it is, why it happens and what you
(00:21):
actually do about it. Make it stick.
OK, let's start right at the beginning then.
What is Urticaria, clinically speaking?
Well, fundamentally it's a skin thing.
You get this sudden onset of raised itchy areas on the skin.
Wheels we call wheels, right? And the crucial bit?
They're transient. They appear, they itch, and then
(00:42):
they, well, they disappear from one spot usually within hours,
certainly less than 24 hours typically.
Transient. OK.
And what do they look like, these wheels?
You're generally looking for itchy bumps, papules, or maybe
larger patches. Plaques, often pale or white in
the middle and surrounded by redness.
That's the erythematous flare. Size and shape can vary quite a
(01:03):
lot though. Yeah, OK.
And angioedema often comes up alongside urticaria.
How does that fit? Up.
Yeah, they often go hand in hand.
Urticaria, the wheels, that superficial skin swelling.
Angioedema is deeper, deeper swelling.
Exactly. Deeper layers of the skin.
Sometimes, because membranes too, like lips or eyelids, it
might feel more tight or even a bit painful, rather than just
(01:25):
intense, intensely itchy like the wheels.
You can get both together, or sometimes just one or the other.
Got it. So wheel superficial angioedema
deeper and I remember there's a classification based on how long
it lasts. Yes, very simple.
Acute urticaria is anything lessthan six weeks, OK.
And chronic urticaria is when ithangs around for six weeks or
more. That time scale is really the
(01:46):
key split. Six weeks.
Got it. So what's actually going on
under the skin? What's the the aetiology the
'cause? Right, the core mechanism is all
about about mass cells in the skin.
They get activated immune cells.Right, yes, and when they get
triggered, they release a whole load of chemicals.
The big one everyone knows is histamine.
Histamine, hence antihistamines being the go to treatment
(02:07):
precisely so histamine and otherinflammatory stuff get released
and they affect the tiny blood vessels nearby the capillaries.
They make them leaky. Leaky capillaries and that
causes the swelling. You got it.
Fluid leaks out from the blood vessels into the skin tissue
causing that raised area of the wheel, and the histamine
(02:28):
directly hits the nerve endings,which is why it's so incredibly
itchy. OK mast cells pop, release
histamine, vessels leak, skin puffs up and itches like mad.
What makes the mast cells pop inthe 1st place?
What are the triggers? The list is pretty long.
You've got your classic allergens, certain flights,
maybe insect stings, some medications.
Right, the allergic stuff. But interestingly, it's often
(02:50):
not allergic. Physical factors are really
common triggers like what thingslike pressure on the skin, but
from tight clothing or sitting, cold, heat, sunlight, even
vibration or exercise can trigger in some people.
Infections are another big one. Viral infections, sometimes
bacterial stress, definitely a factor, and sometimes there's an
underlying autoimmune process going on.
(03:11):
That's a massive range. It is and a really important
point. Especially we talked about
chronic urticaria. Often we actually can't find a
specific trigger, it just seems to happen idiopathic or
spontaneous. Right, which must be incredibly
frustrating for patients, Absolutely.
So are some people more likely to get this?
Any specific risk factors we should know?
(03:33):
Yeah, there are a few things. Having a history of other
allergic conditions, what we call atopy.
So eczema, asthma, hay fever that makes you more prone?
OK, the etopic link. A family history of urticaria or
other allergies also increases risk and certain underlying
medical conditions, particularlyautoimmune diseases.
Thyroid disorders are quite commonly linked, for example.
(03:54):
Right, so a history of allergiesor autoimmunity flags higher
risk. Let's just quickly revisit the
how the pathophysiology mast cells histamine leaky vessels.
Yeah. So just to nail that down,
histamine and the other chemicals cause vasodilation.
The blood vessels widen and crucially, they become more
permeable. Permeable.
Leaky. Exactly like tiny garden hoses
(04:15):
suddenly springing leaks, fluid seeps out into the surrounding
tissue. That fluid collection is the
wheel, and it happens fast and usually resolves fast too as the
histamine gets broken down. Great analogy of the leaky
hoses. Is the basic mechanism the same
if it's, say, a peanut allergy versus being triggered by cold?
Well, the end result is the same.
The mast cell releases its contents.
(04:36):
You get the leaky vessels, the wheel, the itch.
The difference is how the mast cell gets that initial signal.
Allergic urticaria typically involves the immune system's Ige
antibodies recognising the allergen and telling the mast
cell to degranulate. But non allergic triggers like
cold or pressure, they seem to activate the mast cell through
different pathways, ones that don't necessarily involve Ige.
(04:59):
Different roads leading to the same mast cell activation makes
sense now. Differential diagnosis super
important. Someone comes in itchy with
raised bits. What else must be on your radar?
Well, absolutely vital because things can look similar.
Obviously IG edoema is on there.As we said, it can happen alone,
but think about dermatitis or pettiformis.
That's the coiliac related one, right?
Blisters, exactly. Intensely itchy little blisters,
(05:20):
often on elbows, knees, buttocks.
Then there's pemphagoid, anotherblistering condition, usually in
older people. Iris syphilis.
That's a bacterial infection. Usually red, hot, swollen, well
defined edge, often with fever. Doesn't tend to come and go like
Urticaria. Right, infection looks
different. What else?
Eczema can be itchy and red, of course, but the skin changes are
usually drier, maybe scaly, and they stick around the same
(05:43):
place. They're not transient like
wheels or to carry a pigmentosa.That's actually a type of
mastocytosis where you have too many mast cells.
Looks like brownish spots that turn into wheels if you rub
them. Chronic pruritus is just the
medical term for long term itching without the specific
rash of urticaria. Just.
Itching. Yeah, and polymorphic eruption
of pregnancy. PEEP or PUPPP as it used to be
(06:05):
called. Very itchy rash usually starts
in stretch marks specific to pregnancy.
Definitely one to remember for pregnant patients for sure.
And the last one, which we really need to highlight is
urticarial vasculitis. Right, you mentioned this.
How is it different and why is it so important to spot?
OK, so standard urticaria is leaky vessels.
Urticarial vasculitis is inflamed blood vessels.
(06:28):
The vessel walls themselves are inflamed.
Inflammation, not just leakiness.
Exactly. And that changes things.
The lesions in vasculitis often feel more painful or burning
rather than just inchy. They might feel a bit bruised
and critically, they last longer, usually more than 24
hours. Somebody's days.
They might even leave a faint bruise like mark or pigmentation
(06:48):
behind when they finally fade. So pain persistence over 24
hours, maybe bruising Clues for vasculitis?
And why is spotting it so crucial?
Because it's a sign of actual blood vessel inflammation, it
can be linked to underlying systemic problems, connective
tissue diseases, other autoimmune conditions, sometimes
infections, or even medications.It needs a different workup.
(07:11):
You almost always need a skin biopsy to confirm it, which you
wouldn't routinely do for simpleurticaria.
OK, that's a really key distinction.
Urticaria, itchy, transient, leaky vasculitis, painful,
persistent, inflamed, needs biopsy.
Got it. How common is plain old
urticaria epidemiology? It's very common here in the UK
(07:31):
and globally. Lifetime prevalence, The chance
of getting it at least once is thought to be around 20%.
Wow, one in five people. That's huge.
Yeah. Is that mostly the short lived
type? Yes, that 20% is mainly acute
urticaria. Chronic urticaria lasting over
six weeks is much less common, maybe around 2-3 percent
lifetime prevalence, so most episodes are brief.
OK. Acute is common, chronic is less
(07:52):
so any particular groups affected more?
Acute tends to be seen more in kids, adolescents and women
particularly. Those are the atopic background,
the eczema, asthma crowd. Chronic urticaria is a bit more
common in adults, generally OK. Thinking about seeing a patient
again, What are the absolute must know clinical features?
The core things. Two things raised itchy, pink or
(08:14):
red raised skin lesions that arepuritic, meaning itchy.
Raised and itchy? Yep.
Remember they vary in size and shape, might have that pale
centre and they disappear from one spot within 24 hours.
That transience is key. Can be anywhere on the body.
May or may not have associated angioedema.
And we talked about the clinicalsubtypes, particularly for
chromic. Right.
So acute often has no obvious cause found, but think triggers
(08:39):
allergies, infections, physical stimuli.
For chronic lasting over six weeks, you've got chronic
spontaneous urticaria. That's the one with no clear
external. Trigger exactly those stress or
underlying low grade infections might play a part than
autoimmune urticaria linked to other autoimmune conditions
where the body's own antibodies trigger the mast cells.
(09:00):
OK an inducible urticaria. This is where specific physical
things reliably bring on the hives.
Right, like the examples you give cold pressure.
Yeah, delayed pressure urticaria, cold urticaria, solar
urticaria from the sun, heat urticaria, demographism, the
skin writing one. These are all inducible types.
The history points you strongly towards them.
So if someone says every time I carry heavy shopping bags my
(09:22):
hands swell and where the handles were, you'd think.
Delayed pressure urticaria. Exactly.
History is everything for the inducible types.
And again, just to keep it in mind, Urticaria vasculitis looks
like urticaria, but remember those differences.
Pain last 24 hours, maybe bruising needs that biopsy
confirmation. Got it.
History. History.
History. So how do we actually diagnose
(09:45):
this? Do we need loads of tests?
What investigations? OK, key.
Point number one for investigations, diagnosis is
primarily clinical. Based on the story and what you
see. Exactly, history and examination
are paramount. You don't usually need a battery
of tests for straightforward acute urticaria.
So no routine bloods for everyone.
Generally no. Investigations are guided by the
(10:06):
history and clinical picture. You tailor them.
For example, if the story suggests an infection might be
the trigger, then yeah, maybe a full blood count.
Check inflammatory markers like ESR or CRP?
OK. Liver function tests?
Maybe if there are other signs suggesting systemic illness?
What about finding a specific trigger like the physical ones?
If you suspect an inducible type, you might do specific
(10:28):
challenge tests in clinic, like carefully applying an ice cube
to test for cold urticaria or controlled pressure from
pressure urticaria. Dermographism is easy to test,
just gently stroke the skin and see if a wheel forms.
The skin writing test. Simple.
Yep, if you suspect a true allergy, especially in acute
severe cases, then allergy testing might be indicated.
(10:50):
Skin prick tests or specific Igeblood tests for suspected foods
or venoms. For instance, patch testing
might be used for suspected contact triggers.
And if you're thinking autoimmune?
Then testing for things like thyroid auto antibodies could be
relevant, especially in chronic spontaneous urticaria.
Given the known link, sometimes the best test is simply stopping
(11:11):
a suspected medication or avoiding A suspected food
trigger and seeing if things improve.
Right, a therapeutic trial. What about things like H pylori
testing or urine tests? When did they come in?
H pylori testing is sometimes considered for chronic
spontaneous urticaria, particularly if there are
digestive symptoms, as eradicating it might help a
small subset of people. A urine dipstick might be done
(11:33):
if you're worried about kidney involvement, maybe hinting at a
systemic cause. Or again, urticariovasculitis,
which can sometimes affect otherorgans.
And the skin biopsy? Reserved almost exclusively for
when you suspect urticariovasculitis to look for
that blood vessel inflammation under the microscope.
So investigate smartly, based onsuspicion.
Don't just order everything makes sense.
(11:55):
Let's talk management. What do we actually do?
First step, if you can identify a trigger is obviously
avoidance. Seems simle but crucial.
Avoid the trigger. Yeah, and atient education is
key advise about potential nonspecific worsening factors.
Things like getting too hot, stress, alcohol, caffeine.
Sometimes NS is like ibuprofen, can make it worse even if
(12:16):
they're not the primary cause. OK, general advice.
What about for the itching itself?
Symptomatic relief. You can use topical things like
calamine lotion or creams containing menthol for cooling
effect. Simple but can help.
But the mainstay, the core medical treatment, is
antihistamines. The H1 blockers.
Yes, specifically the non sedating or low sedating H1
(12:38):
antihistamines. Think cetirizine, loratadine,
fexofenadine. They block histamines effects
reducing the itch in the wheels.That's first line.
And what if a standard dose, say10 milligrammes cetirizine isn't
cutting it? This is really important for
chronic urticaria management guidelines like NICE here in the
UK recommend increasing the doseof the non sedating H1
(13:00):
antihistamine. Increase the dose, How much?
You can go up to four times the standard licence dose, so for
example up to 40 milligrammes ofcetirizine or loratadine per
day. This often gets control when
standard doses fail. OK so push the first line drug
dose up before adding something else.
Good tip. What about really bad flare ups?
Acute severe hives. For those situations, a short
(13:21):
course of oral steroids like Prednisolone can give rapid
relief, usually just for a few days, maybe a week.
Quick fix? Yeah, a rescue course, but you
want to avoid long term steroid use because of all the side
effects. Absolutely.
So what happens if someone has chronic urticaria, they're on
four times the normal antihistamine dose and it's
still not controlled? What are the second line
options? Right, this is usually moving
(13:43):
into specialist territory or at least discussion with a
specialist. Options might include adding in
an anti leukotriene drug like model Lucast or move into
biologic therapy with omolizumab.
That's an injection an anti Ige antibody.
Quite effective for many with difficult chronic spontaneous
urticaria. Molizumab.
And for really tough refractory cases, immunosuppressants like
(14:06):
sicklosporin or sometimes otherslike mycophenolate or tacrolimus
might be considered, but these need careful monitoring and
specialist management so. Let's do a quick scenario.
Patient chronic hives, daily disruption.
Tried cetirizine 10 milligrammesand 20, then 40 milligrammes
daily. Still bad?
What's likely the next step? So after maxing out the non
(14:26):
sedating antihistamine dose likethat, the next typical step
often view a referral would be to consider adding omalizumab or
possibly cyclosporine. Clear pathway?
When else should you definitely refer?
OK, referral triggers, diagnosisis uncertain, symptoms aren't
controlled Despite that antihistamine dose escalation.
If they need continuous antihistamines for more than six
weeks and primary care feels stuck, definitely.
(14:49):
If you suspect urticariovasculitis, they need
that confirmation makes sense and urgent hospital admission.
Of course, if acute urticaria israpidly worsening, especially if
there's angioedema involving thethroat or tongue, or any signs
of anaphylaxis. Fairway, compromise.
Emergency. Absolutely.
Also severe acute urticaria where you strongly suspect a
(15:10):
food or latex allergy needs urgent assessment because of
that anaphylaxis risk. And sometimes really challenging
Inducible urticaria is like severe solar or cold urticaria
might need specialist input for management strategies.
OK, so identify triggers and histamines first, escalate dose
steroids for flares, then specialist options and know when
(15:31):
to refer or admit urgently. What's the long term outlook?
The prognosis? Depends hugely on acute versus
chronic. For acute urticaria, prognosis
is generally excellent. It's usually self limiting,
resolves in days or weeks, responds well to treatment.
Good news for most people then. What about the chronic form?
Chronic Urticaria. It's more persistent, more
(15:53):
unpredictable. The good news is about half of
people find their symptoms resolved within about three to
five years. OK, half get better.
Eventually a significant minority, maybe around 20%, can
still have symptoms even a decade later.
It's going to be a really long term burden for some.
Wow, a decade? Are there clues about who might
have it longer? Yes.
Factors that suggest a potentially poorer prognosis for
(16:16):
chronic spontaneous urticaria include having more severe
symptoms to start with, having angioedema alongside the wheels
and interestingly testing positive for those anti thyroid
antibodies we mentioned earlier.The autoimmune link again.
Finally, any major complicationsto worry about?
Serious physical complications are pretty rare with urticaria
itself, unless it's part of anaphylaxis.
(16:37):
But the main complication, especially with chronic
urticaria, is the impact on quality of life.
Which sounds significant. Hugely constant in the
unpredictability. The appearance changes with
angioedema. It can lead to really
significant sleep problems, insomnia.
I can imagine. And psychological distress,
anxiety, even depression are unfortunately common in people
living with severe chronic urticaria.
(16:58):
Makes total sense. Anything else?
Just to reiterate, while anaphylaxis is rare from chronic
spontaneous urticaria itself, it's always a potential risk if
the urticaria is an early sign of a severe acute allergic
reaction to something specific like a food, drug or sting.
So vigilance for systemic symptoms is always important in
(17:18):
acute onset. Right.
Always keep anaphylaxis in mind with acute hives.
OK? That covers a huge amount from
the basic definition and the leaky capillaries through
friggers, differentials like vasculitis, the investigations,
the step management, prognosis and impact.
It really shows how understanding that basic pathway
mast cell histamine leaky vessels unlocks, why it looks
(17:40):
the way it does, why it itches, and why antihistamines are the
first step in treatment. And remembering those key
differences like the transience versus persistence for
vasculitis and knowing the management pathway, especially
that antihistamine dose escalation.
It might be common, but getting the diagnosis and management
right is crucial. Absolutely.
It's about having that structured approach when you
encounter it. That was a fantastic deep dive
(18:02):
into your urticaria. Really high yield stuff.
Agreed, hopefully that sets you up well, whether it's for exams
or for seeing patients. For more free MSRA revision
resources, visit freem-sra.com and for the full Premium
Revision Toolkit, head to pass the m-sra.com.
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