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Welcome to the Deep Dive.
If you are preparing for advanced practice, well, you're going to encounter allergies a lot.
Oh, absolutely, almost daily in many settings.
So today we're cracking open chapter 46.
It's really the playbook for handling these exaggerated immune responses, right, focusing on allergic rhinitis and those real emergencies.
Exactly.
And it's crucial stuff.
The word allergy itself comes from Greek,
allos meaning differing from normal, and ergon, which is work or energy.
So abnormal energy release.
Pretty much an exaggerated unwanted immune response.
Our mission today is to really get a handle on classifying these reactions and importantly controlling them with pharmacology.
Okay.
And it all stems from an antibody antigen reaction, doesn't it?
That's the core mechanism.
Let's start with that Coombs and Gell classification then.
It sort of sets the stage for everything.
Four types of hypersensitivity.
That's right, four types.
And type one, that's the immediate hypersensitivity, the one we often think of first.
Why immediate?
What's happening there?
It's driven by IgE antibodies.
They bind to mast cells and basophils.
Then when that same allergen comes along again.
Ooh, degranulation.
Right.
The cells just dump histamine, locutrenes, prostaglandins,
all those chemical mediators.
And that's what causes the immediate symptoms, like an asthma or allergic rhinitis.
Precisely.
That immediate cascade.
Okay.
Type one is clearly a big focus for management.
Can we quickly outline the other three, just for context?
We need to know they exist before we dive deep into treatment.
Sure.
Quick overview.
Type two involves IgG antibodies attached to a T lymphocyte killer cell.
Think cytotoxic reactions, like immediate blood transfusion reactions.
Got it.
Type three.
Immune complexes.
They get deposited in tissues, cause damage.
You see this in autoimmune diseases like lupus, systemic lupus or osemitosis.
Okay.
And type four, that one's different, isn't it?
Delayed.
It is.
It's T -cell mediated, not antibody mediated.
That's why it's delayed hypersensitivity.
It takes two to seven days to show up.
Like poison ivy.
That rash that appears days later.
Perfect example.
Classic contact dermatitis.
Okay.
That framework is helpful.
But let's pivot to the most dangerous type one reaction,
anphylaxis.
This isn't just symptoms.
It's a systemic meltdown.
Catastrophic is the word.
You get this rapid, massive, systemic release of all those mediators we mentioned.
Histamine, leukotrienes, everywhere.
Leading to what?
Physiologically?
Aggressive vasodilation.
Blood vessels widening everywhere and increased capillary permeability.
Fluid just rushes out.
Out of the bloodstream.
Exactly.
So your effective plasma volume plummets.
You get hypertension shock.
At the same time, smooth muscles contract.
So you get bronchospasm, airways closing.
Decreased oxygenation.
It's a perfect storm.
It is.
And if you don't intervene immediately, it can be fatal very quickly.
Intervention means epinephrine.
First, last, always.
Absolutely.
Epi is the cornerstone, non -negotiable.
And the crucial clinical parole for administration?
Where does it go?
Location, location, location.
It must be an intramuscular and IM injection.
And specifically into the lateral thigh muscle.
The vastus lateralis.
Why there?
Why not subcutaneous or the arm?
Fastest absorption.
Shortest time to peak concentration.
Subcutaneous is slower.
The deltoid muscle in the arm is slower.
And anaphylaxis is faster.
Everything.
Epi reverses the vasodilation.
Brings blood pressure back up.
Okay, lateral thigh.
Got it.
What about other things we might give, like Benadryl or an albuterol nebulizer?
Those are adjuncts.
Secondary.
Injectable davenhydramine, say 25 to 50 milligrams for an adult.
Helps with itching, hives, the skin stuff.
Nebulized albuterol, maybe 2 .5 to 5 milligrams, can help with the bronchospasm, the airway obstruction.
But they don't fix the core problem.
Correct.
Critically important.
They alone do not treat the underlying hypotension or the shock.
Epi does that.
These help with symptoms.
So epi first, lateral thigh.
Then we think about the massive fluid shift and all that capillary leakage.
Right.
You need rapid IV fluids to replace that lost volume.
Normal saline usually, maybe 1 to 2 liters is a bolus, sometimes more.
And corticosteroids, like mesopendicillone.
We often give those two,
yes.
Systemic corticosteroids, maybe 1 to 2 milligrams per kilogram per day.
But understand their role.
They're not for the immediate crisis.
They take 4 to 6 hours to really kick in.
Their job is to help prevent a potential late phase reaction hours later.
They don't help with the immediate shock or breathing issues.
Okay, that clarifies the sequence.
Epi, fluids, then consider steroids for later.
Let's shift gears from that acute disaster to the chronic nuisance.
Allergic rhinitis.
Hay fever.
Ah, yes.
If anaphylaxis is the system completely overloading, rhinitis is more like the system just constantly sputtering out those mediators.
That's a good way to put it.
We usually talk about seasonal versus perennial.
We do.
Seasonal is the classic hay fever.
Symptoms line up with pollen seasons, trees in the spring, grasses in the summer, weeds in the fall.
Ragweed is a huge culprit for many people.
And perennial.
That's year -round misery.
Usually triggered by indoor stuff, dust mites, animal dander, maybe molds.
Avoidance can be tougher for these folks.
Diagnosis.
Besides the history, what physical signs might we see?
The telltale signs.
You look for the classics.
Those allergic shiners, the dark circles under the eyes from venous congestion, pale swollen nasal passages, maybe kind of bluish,
often with clear watery discharge.
And sometimes that little horizontal crease across the nose bridge,
the allergic solute from constantly rubbing upwards.
Right.
And to confirm what they're allergic to, skin testing is common.
The scratch or prick test.
What's the absolute must -do for patients before this test?
Stop their antihistamines.
This is critical.
Oral H1 blockers need to be stopped.
Usually 48 to 72 hours beforehand, otherwise you risk a false negative.
Because the antihistamine will block the reaction you're trying to provoke.
Exactly.
You're looking for that wheel and flare reaction, which should pop up in 15 to 30 minutes if it's positive.
Can't see it if the antihistamine is blocking it.
What if stopping isn't feasible?
Like for a young kid or someone with really bad hives or eczema?
Then we can turn to blood tests.
Specifically, the RAH test, radioallergic assorbent test.
It measures specific IgE antibodies in the blood.
Is it as good?
It's generally less sensitive than skin testing and often more expensive.
But it's a valuable alternative when skin testing is impractical or safe.
Okay.
Let's talk management.
The goal is symptom relief with minimal side effects, mostly by targeting those H1 receptors.
There's a stepwise approach, often shown in tables like 46 .6.
What's at the top?
What's the powerhouse?
Intranasal corticosteroids, ICS.
They are hands down the most potent agents we have for established rhinitis.
They should be first line therapy.
Why so potent?
What makes them the king?
They hit the inflammation broadly.
They inhibit multiple inflammatory cell types, mast cells, eosinophils, others, and they reduce multiple mediators.
Not just histamine, but also leukotrains.
They basically calm the whole inflammatory cascade down.
Okay.
Broad action.
But they aren't instant relief, are they?
Patients need to understand the timing.
Definitely not instant.
Some effect might start in, say, 3 to 12 hours.
And this is key.
Maximal benefit takes consistent daily use for one to two weeks.
So counseling is vital, especially for seasonal allergies.
Absolutely.
You need to tell patients to start their ICS two to four weeks before their usual allergy season kicks off.
Prophylaxis is key.
What about side effects?
People hear steroids and worry.
Are systemic effects a big issue with these nasal sprays?
With the standard doses of drugs like fluticasone or mometazone, systemic absorption is actually very low.
So major systemic side effects are uncommon.
What do patients experience sometimes?
Mostly local stuff.
Neasel irritation,
maybe some dryness, occasional nosebleeds, skinging.
The concern about growth suppression in kids has been studied extensively, and at recommended doses the risk appears minimal, if any.
Good to know.
Now what if someone is so congested they feel like the spray isn't even getting up there, like in some case studies?
That's a practical problem.
For the first two or three days, they can use a topical nasal decongestant spray like
oxymetazoline just before the steroid spray.
To clear the path.
Exactly.
Shrink the swelling, open things up so the corticosteroid can actually reach the nasal TQs effectively.
Just for a few days though.
Right.
We'll come back to why only a few days.
Let's move to second line, antihistamines, H1 blockers.
Big difference between the older first generation and the newer second generation.
Huge difference.
The first gen drugs, like defenhydramine, Benadryl,
or chlorphenamine, they work well, block histamine effectively, but they readily cross the blood brain barrier.
That means sedation, sometimes significant sedation, and they have strong anticholinergic effects.
Meaning dry mouth, blurry vision.
Dry mouth, blurred vision, constipation, urinary hesitancy, confusion, especially in older adults.
Big problems.
No, definite populations to avoid them in.
Oh yes.
Contraindicated in breastfeeding mothers.
Used with extreme caution, or better yet avoid, in the elderly.
People with narrow angle glaucoma, it can raise eye pressure, and men with BPH, benign prostatic hyperplasia, as it can cause urinary retention.
Plus tolerance can develop.
Okay.
So along came the second generation antihistamines, the NSA's non -sedating agents, loratadine, claritin, fexofanadine, the like.
Right.
These were designed to be less lipophilic, meaning they don't cross the blood brain barrier as easily.
Resulting in?
Much less sedation, minimal anticholinergic side effects.
Way safer for older adults, people who need to be alert.
They're generally preferred for routine use.
Are any of the second gens known for being a bit more sedating than others?
Yes.
Satirazine, Zyrtec, and his isomerolivocitrazine, dialsyl, are known to have a slightly higher potential for sedation compared to loradadine or fexofanadine.
Although still much less than the first gen drugs.
Something to keep in mind.
Good distinction.
Okay.
Next category, nasal decongestants, the sympathomimetics.
They shrink swollen tissues.
They do, by causing visoconstriction.
Oral versions like pseudoephedrine, sudafed, and phenolaphrine, they work systemically.
Which means systemic side effects.
Exactly.
They act like CNS stimulants.
It can cause increased blood pressure, increased heart rate, palpitations, insomnia, nervousness, irritability.
This brings us back to case study two's lesson.
Who really needs to avoid these oral decongestants?
Huge caution flags for anyone with hypertension,
especially uncontrolled hypertension, heart disease, hyperthyroidism, or narrow angle glaucoma, and an absolute contraindication if someone is taking an MAO inhibitor.
Why MAOIs?
Risk of a hypertensive crisis, a dangerous rapid spike in blood pressure.
It's a critical interaction to avoid.
Now what about the topical decongestant sprays?
The ones that give that fast, amazing relief.
They work great initially, like oxometazolene, aphrine.
Fast, dramatic relief.
But there's a catch, a big one.
The infamous rebound congestion, rhinitis medicamentosa.
If you use them for more than three or maybe four days max, the nasal tissues become dependent.
When the spray wears off, the congestion comes back even worse than before.
It creates this vicious cycle of needing the spray more and more often.
Making them totally impractical for chronic allergies.
Totally.
Good for a very short -term fix, like that initial blockage before starting an ICS, but not for ongoing use.
Okay, quickly, third line or prophylactic options, intranasal chromalin.
Chromalin sodium.
It's a mast cell stabilizer.
It prevents the release of histamine.
Key word, though, is prevents.
So not for acute symptoms.
No value for acute symptoms.
It has to be used prophylactically, starting maybe two to four weeks before exposure, and continuously, often four times a day, needs commitment.
Right.
And for those who really fail avoidance and medications.
Immunotherapy is an option.
Allergy shots.
It's a long -term commitment, injecting small amounts of the allergen over years, usually three to five years, to desensitize the immune system.
Retraining the immune system.
Essentially, yes.
Yeah.
And we're seeing newer forms too, like pelforzia, that oral immunotherapy powder for peanut allergy.
What's the critical point about starting pelforzia?
High risk of anaphylaxis.
So the initial dose escalation, and actually all dose increases, must happen in a supervised healthcare setting, equipped to handle severe reactions.
Patients have to be in a REMS program, risk evaluation, and mitigation strategy.
Okay.
Safety first.
Before we wrap, let's touch on special populations.
Pregnancy.
What's generally considered okay?
Intranatal steroids like sleuticosone and ometisone are often preferred because their systemic absorption is so low.
For antihistamines, loratidine and cetirizine are generally considered acceptable, as is defenhydramine for occasional use, though sedation is a factor.
What about decongestants during pregnancy?
Oral decongestants, especially pseudoepithedrine, should really be avoided, particularly in the first trimester, due to potential risks.
And managing kids versus older adults?
Pediatrics obviously requires careful dosing based on weight or age.
For geriatrics, you have to be mindful of slower metabolism and increased sensitivity to side effects, particularly the CNS and anticholinergic effects of first -gen antihistamines.
Tailoring is key.
Start low, go slow.
This has been a really thorough walkthrough.
If you had to boil it all down, what are the absolute top three clinical takeaways for our learners managing allergies?
Okay.
Three anchors.
One,
intranasal corticosteroids are your most potent first -line therapy for established allergic rhinitis.
Start there for consistent symptoms.
Got it.
Two.
Always favor the second -generation non -sedating H1 blockers over the older first -generation sedating ones due to side effect profiles, especially anticholinergic burden.
Makes sense.
And three.
Three.
In an acute life -threatening crisis, anaphylaxis epinephrine is paramount.
Administered IM in the lateral thigh, everything else is secondary to that immediate action.
Perfect summary.
And listeners, remember, monitoring goes beyond just, are your symptoms better?
As box 46 .3 highlights, we need to ask about quality of life.
Are side effects like sleepiness impacting school or work?
Is the cost okay?
Are they actually taking it?
That's holistic care.
Couldn't agree more.
Yeah.
So maybe a final thought to chew on.
Avoidance is technically the first step, right?
Especially for indoor things like dust mites and pet dander.
But we know patients often say removing a pet is, well, unacceptable.
Yeah, that's a tough one.
So the challenge for you is, what practical specific steps can you realistically coach your patients through to reduce that allergen load at home, even if the pet stays?
Because making pharmacotherapy work often relies heavily on chipping away at that environmental exposure too.
A very real -world clinical puzzle.
Excellent point to end on.
Thanks so much for walking us through all of this.
My pleasure.
And thanks everyone for joining the Last Minute Lecture team for this deep dive.