Chapter 32: Sore Throat Assessment & Diagnosis

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Hello and welcome back to the Deep Dive.

You know, there's this paradox in primary care that I think drives every clinician a little bit crazy.

Oh, I think I know where you're going with this.

It is the condition that brings everyone in,

is universal, it is annoying,

and honestly, 90 % of the time, it is gonna go away on its own with some tea and honey.

The sore throat.

The sore throat, pharyngitis.

But here is the paradox.

While most of it is just a viral annoyance, hiding inside that massive haystack of runny noses and scratchy throats are these needles that can actually kill you.

They really can.

We're talking airway obstruction, and deep neck abscesses, rheumatic heart disease.

It is the classic needle in the haystack problem.

And honestly, that is why we have jobs.

If it were just about handing out lozenges, a kiosk could do it.

But spotting that one autoglutitis case in a sea of viral poles, that requires a very specific, very disciplined system.

And that is exactly our mission today.

We are taking a deep dive into chapter 32 of Advanced Health Assessment and Clinical Diagnosis in Primary Care, the sixth edition.

A great chapter.

It is.

And I'll be honest, when I first looked at this chapter, I thought, do we really need an entire hour on sore throats?

Well, did you decide?

And I was wrong.

Because this text lays out a roadmap that is so much more sophisticated than just strep versus not strep.

It gives us a mental framework to make sure we never, ever miss those dangerous needles.

It really does.

And the text emphasizes right off the bat that we have to move beyond just pattern recognition.

You know, that looks red.

Here's an antibiotic.

Right.

And move toward actual diagnostic reasoning.

We're gonna cover everything from the pathophysiology and the scary emergencies to the nitty gritty of the physical exam.

And speaking of the exam, there's one concept in this chapter, I call it the big divider, that completely changed how I visualize the aura pharynx.

I know exactly what you're talking about.

It's the classification method the chapter introduces almost immediately.

The first major mental branch for the clinician is sorting sore throats into two categories.

The char.

Pharyngitis with ulcers and pharyngitis without ulcers.

It sounds so basic, doesn't it?

Ulcers versus no ulcers.

It does, but think about the cognitive load it saves you.

As soon as a patient opens their mouth, that is your first decision node.

Do I see lesions and breaks in the mucosa or is the mucosa intact but inflamed?

If you see ulcers, you have immediately swept half the differential diagnosis off the table.

Exactly.

You weren't worrying about strep or mono primarily.

You are now hunting for herpes, cocksacky, or maybe something fungal.

Precisely.

It turns a broad fuzzy problem into a binary decision tree.

And that is what we wanna do today.

Build that tree in your head so it's automatic.

Before we start climbing that tree though, let's get our hands dirty with the basics.

Pathophysiology 101.

Okay.

What is actually happening in the tissue when a patient says, Doc, it hurts to swallow?

So fundamentally we are dealing with pharyngitis.

This is inflammation of the mucosa of the aura pharynx.

The tissues are edematous, meaning swollen with fluid.

They are hyperemic, that's the redness from increased blood flow, and the nerve endings are being irritated.

And usually some invaders causing that party.

Right.

And the text is very clear on the usual suspects.

The vast majority are viral.

We're talking adenovirus, influenza, parainfluenza, cocksacky A viruses.

All the common colds.

All the common stuff.

These pathogens invade the mucosal cells, replicate and trigger that local immune response.

Which is why we get the swelling and the pain.

But then we have the bacterial side, which is smaller, but I guess louder.

Louder in our minds for sure.

The bacteria,

group A beta hemolytic streptococcus GSS.

That is the one we are all obsessed with.

We really are.

It's less common than people think though.

The text notes it's only about 10 % of adult sore throat visits.

Only 10%.

That feels low considering how many prescriptions are written for in this country.

It is remarkably low compared to prescribing habits.

In kids, it's higher up to 30%.

But that still means 70 % of kids with sore throats do not have strep.

So even in the peak population, it's still the minority.

It is.

There is a fascinating little note in the pathophysiology section about referred pain.

I think this trips up a lot of students.

The patient points to their throat, but the throat looks fine.

This is pure anatomy.

The pharynx shares nerve innervation with other structures.

The glossopharyngeal nerve, cranial nerve IX does a lot of work here.

So pathology in the ears, like in otitis media, can present as throat pain and vice versa.

Or the thyroid.

The book mentions the thyroid.

Or the thyroid, absolutely.

Subacute thyroiditis can present as anterior neck pain that mimics a sore throat.

So if the pharynx looks pristine, you have to widen your lens.

You'll have to look elsewhere.

You really do.

So we have this landscape, mostly viral, sometimes bacterial, sometimes referred pain.

But here is the million dollar question.

Why do we care?

If 90 % are viral, and even strep is usually self -limiting, why are we doing this rigorous deep dive?

Why not just treat symptomatically and wait?

That is the so what question.

The text is explicit here.

We care because of the sequelae.

Sequelae, the after effects.

Yes, we aren't treating the sore throat.

We are treating the future complications.

Oh, in defense.

We are.

With group A strep, the specter in the room is acute rheumatic fever.

Which sounds like something from a Victorian novel.

We don't see it much anymore in developed countries.

Thanks to antibiotics and better living standards.

But it hasn't disappeared.

And if you miss a strep case, and that patient develops rheumatic carditis, you are looking at permanent heart valve damage.

And colomero and anaphyritis.

Kidney damage, exactly.

Plus, there are the immediate suppurative complications.

What does that mean, suppurative?

Pus forming.

So peritonsillar abscesses, retrofaryngeal abscesses, these are nasty infections that require drainage and hospitalization.

So the rigorous assessment is really about risk stratification.

We are trying to prevent permanent damage.

All right, so the stakes are set.

Now, let's walk into the exam room.

Section one of our analysis is diagnostic reasoning.

And the text essentially yells at us here.

Before you ask about their fever, before you ask about their sick kids, stop.

Stop and do the emergency check.

Is this patient about to die?

It sounds dramatic, but airway obstruction is a real risk.

You have to clear the death zone first.

The text highlights two major emergencies, epiglottitis and peritonsillar abscess.

Let's talk epiglottitis.

This is the nightmare scenario.

Thankfully, it's rare now, largely due to the Hib vaccine hemophilus influenza type B, but rare doesn't mean gone.

And it can still happen in adults.

Right, it can occur in adults too, often from other organisms.

What does this patient look like?

Paint the picture for us.

They look toxic, and that is a clinical term.

They aren't scrolling on their phone.

They are focused entirely on breathing.

They might be sitting in a tripod position, leaning forward, hands on knees, neck extended.

This is the sniffing position to maximize airway entry.

And the drooling.

The book emphasizes the drooling.

The drooling is key.

They cannot swallow their own saliva because the epiglottis is so inflamed.

It's so painful and swollen, so it just spills out.

I always remember the description of the voice, the hot potato voice.

It's such a specific descriptor, isn't it?

It's muffled.

It sounds like they're trying to talk around a mouthful of hot mashed potatoes.

Why does it sound like that?

That is due to supraglottic swelling, swelling above the vocal cords, dampening the resonance of the voice.

It's muffled at the source.

Now here's a piece of advice from the text that goes against every instinct a doctor has.

You see a patient with a throat problem.

Your instinct is to say, open wide and stick a tongue blade in there to look.

And the text says, do not do that.

Why, what's the risk?

Because that tongue blade, that stimulation of the base of the tongue can trigger a laryngospasm.

A spasm of the voice box.

Exactly.

If that airway is already 90 % closed by a swollen epiglottis, a spasm closes the remaining 10%.

You have just caused a total airway obstruction in your exam room.

Talk about a bad day at the office.

Terrible.

If you see the drooling, the stridor, that high -pitched breathing sound, the tripod posture, do not examine.

You call anesthesia, you call ENT, you get them to a controlled environment where they can secure the airway.

Okay, so hands off the tongue blade for epiglottitis.

What about the other emergency, the peritonsillar abscess or Quinzie?

This is an infection that has broken out of the tonsil and formed a pocket of pus between the tonsil and the pharyngeal muscles.

It's essentially a walled -off infection.

And the hallmark sign here is trismus.

Trismus, lockjaw.

The inflammation irritates the pterygoid muscles, the muscles responsible for chewing, and the patient physically cannot open their mouth fully.

So you ask them to open wide.

And they can only give you a centimeter or two.

That is a huge red flag for an abscess.

So if we see drooling, stridor, or trismus, we are done with the history we are referring.

Correct.

You shift from diagnosis mode to rescue mode.

Your job is to get them to the right place quickly.

But let's assume our patient is uncomfortable but stable.

No drooling, breathing is okay.

Now we get to put on our detective hat.

Section two, the focused history.

This is where we start sifting through the evidence to decide is this viral or is this strep?

And the text suggests starting with the fever pattern.

It's interesting how temperature profiles differ.

Walk us through the strep fever.

Group A strep usually presents with a sudden high fever.

The text specifies greater than 101 .5 degrees Fahrenheit or 38 .5 Celsius.

So it's not a slow build.

No, it's boom, I'm hot.

One minute you feel fine, the next you have a significant fever.

But the flu does that too, right?

True.

Influenza is also abrupt and high can go up to 104.

So high fever alone doesn't differentiate strep from flu perfectly, but it does differentiate them from other things.

Like a mono.

Exactly.

Mononucleosis Epstein -Barr virus is sneaky.

It's insidious.

The fever tends to be low grade.

The patient might not even realize they have a fever at first.

They just feel run down, tired.

And the wild card is Adenovirus.

Ah, Adenovirus is frustrating because it reads the textbook and then does the opposite.

In kids, it can cause a screaming high fever over 104 or they can be completely a febrile.

So it doesn't really follow the rules.

It's all over the map.

So you have to be careful there.

And if there's no fever at all, the patient says, no, I haven't felt warm at all.

If the patient is completely a febrile, you really need to step back from infection as your primary thought.

Think allergies, think candida, think chemical irritation from smoke or GER.

A true bacterial pharyngitis without any fever history is uncommon.

Next on the detective list is exposure history.

That seems obvious.

Is anyone else sick?

But the text puts some hard numbers behind it.

It does.

For strep, the secondary attack rate in families is about 20%.

What does that mean, secondary attack rate?

It means if a sibling has strep, there is a one in five chance this patient has it.

That is a significant likelihood ratio boost.

It makes the diagnosis much more probable.

Whereas mono has a different social network.

Mono is the kissing disease for a reason.

It requires intimate contact saliva exchange.

It's not spreading through aerosol droplets in a classroom the way flu or strep might.

So you have to ask about - You have to ask about dates, shared drinks, that sort of thing, especially in that adolescent and young adult population.

Let's talk about the onset and the quality of the pain.

We mentioned strep is sudden.

Sudden and intense.

Patients will often describe the exact moment it started.

I was fine at breakfast, but by lunch I couldn't swallow my sandwich.

Feels like a switch was flipped.

Exactly.

Contrast that with the insidious onset.

If a patient says, yeah, my throat has been kind of scratchy for a week, maybe getting a little worse, that is rarely strep.

That slow burn points towards viral causes, mono, or even environmental irritants like dry air or smoke.

The book also makes a crucial point about the pediatric history, because a three -year -old isn't gonna tell you, mother, my pharynx is inflamed.

Chuckles, no, they definitely won't.

In toddlers, a sore throat presents as a refusal to eat, the anorexia of pharyngitis.

Ah, so they're just not eating.

They are hungry, they pick up the cracker, and then they put it down because they know it's gonna hurt.

Dehydration is actually a big risk for them, not because of the fever, but because they stop drinking.

Now we're getting to what I think is the most useful part of the history, the rule -out symptoms.

We spend so much time looking for signs of strep, but the text emphasizes looking for signs that it is not strep.

This is the most powerful tool for antibiotic stewardship.

We call them the viral respiratory symptoms.

And what are they?

If a patient has a cough, and if they have rhinorrhea or runny nose, you can almost guarantee it is not group A strep.

That is so counterintuitive to patients.

They cough, they have a runny nose, their throat hurts, and they think, I have a terrible infection, I need antibiotics.

Right, but biologically, group A strep is a localized pharyngeal infection.

It stays in the throat, it does not typically cause bronchial inflammation, which is cough, or nasal mucosal discharge, which is the runny nose.

So it's a throat specialist.

It is.

Those other symptoms are viral behaviors.

The text says the presence of cough and choriza should make you move strep to the bottom of your list.

That's a huge stop sign for prescribing.

What about the eyes?

The eyes can tell a story, too.

Eye symptoms are very specific.

If you see conjunctivitis pink, eye paired with a sore throat, you have to think about pharynconjunctival fever.

Which is a mouthful.

It is.

It's a syndrome caused by adenovirus.

It's a classic pairing.

So if you see the red eyes and the red throat together, think adenovirus.

And on the flip side.

On the flip side, if the eyes are just itchy, watery, and puffy,

that screams allergic rhinitis.

And hoarseness, losing your voice.

Hoarseness implies the inflammation has moved down to the larynx, the voice box.

Again, strep doesn't usually go down there.

Laryngitis is almost exclusively viral or related to vocal strain.

So if they are losing their voice, you can reassure them it's likely viral.

Finally, the systemic checks.

The rest of the body feeling.

If they feel like they've been hit by a truck severe myalgia, body aches think influenza.

Flu hurts everywhere.

And mono.

If it's just overwhelming, crushing fatigue, I can't get out of bed to go to class.

Think mono.

That profound fatigue is a hallmark.

So just by talking to the patient, before we even turn on the otoscope, we have a pretty good idea of where we are heading.

We do.

If they have a sudden high fever and no cough, we're worried about strep.

If they have a scratchy throat, a runny nose, and a cough, we are thinking viral.

But the detective work isn't done.

We have to profile the suspect.

Section three covers patient profile and risk factors.

And age is essentially a filter for your differential diagnosis.

Age is a massive discriminator.

Different mugs, like different ages, it's one of the most useful pieces of data you have.

Start with the little ones, under two years old.

If you see a toddler under two with a fever and respiratory symptoms, do not jump to strep throat.

Why not?

It is extremely rare in that age group.

Their pharyngeal tissues aren't mature enough for the bacteria to adhere well.

The text points to RSV, respiratory syncytial virus, as the main culprit here, or maybe parenfluenza causing croup.

So strep in a one -year -old.

Unlikely.

Very unlikely.

But then you hit the strep belt.

The school -age kids.

Five to 15 years old.

This is the peak incidence for group A strep.

This is where you need to be hypervigilant.

Their immune systems are ripe for it, and they are in crowded classrooms sharing everything.

Then they grow up, go to college, and we enter the mono zone.

Adolescents and young adults.

This is the prime demographic for EBV.

Dorms, shared drinks, dating.

If a 19 -year -old comes in with a sore throat,

mono has to be in your top three.

What about the older adults?

We often forget about them in these childhood illness discussions.

We do, and that's dangerous.

Mono can happen in older adults, but the text warns us it presents atypically.

How so?

They might not have the classic sore throat or swollen lymph nodes.

They might just present with an unexplained fever and liver function abnormalities.

It's much harder to catch.

We also need to get personal with the social history.

We have to ask about things that might make the patient uncomfortable.

We have to ask about sexual practices.

It's standard of care.

It's part of a complete history.

Specifically, or a genital contact.

Correct.

Gonococcal pharyngitis gonorrhea of the throat is a real thing.

The text notes it is present in about 10 % of patients who have genital gonorrhea.

And what does it look like?

And here's the kicker.

It often looks exactly like viral pharyngitis.

It can be asymptomatic or just mildly sore.

So if you don't ask, do you engage in oral sex?

You will never diagnose it.

And you will send them home with a Z -Pak that doesn't treat gonorrhea effectively and the chain of transmission continues, you have to ask.

Okay, what about medical history?

Chronic conditions.

Immunosuppression is a big one.

If a patient is on chemotherapy or has HIV or is on chronic steroids, the rules change.

Their immune system is weakened.

And that opens the door for?

For opportunistic infections.

They are at high risk for fungal infections like candidiasis or thrush and severe viral outbreaks like herpes.

And speaking of medications, the text flags a common one.

Inhaled steroids.

Asthma inhalers, fluticasone, goutsnide.

If patients don't rinse their mouths after using them, the steroid suppresses the local immune system in the throat and yeast overgrows.

And you get thrush.

You get thrush.

It's a very common side effect if they aren't coached on proper technique.

And one last chronic condition that mimics a sore throat perfectly, GERD.

Ah, the silent reflex.

Acid comes up the esophagus while they sleep, irritates the posterior pharynx.

So they don't even feel heartburn.

Not always.

They just wake up with a sore throat that gets better as the day goes on.

No fever, no nodes, just a braining throat every morning.

Okay, we have built a massive profile.

We know the history, the risks, the age factors.

Now it's time to look.

Section four, the physical examination.

This is where the rubber meets the road.

And remember, we start with that general assessment.

Reverify safety.

If they look scary, stop.

Assuming they are safe, we grab the light and we go back to your big divider.

We are on the ulcer hunt.

We are looking for holes in the mucosa.

And the text gives us a great breakdown of what different ulcers look like and where they live.

Location, location, location.

Let's start with the posterior mouth.

Soft palate and uvula.

If you see small grayish vesicles or ulcers, specifically on the soft palate and uvula, and it's the summer or early fall, think herpangina.

Which is caused by?

Cuxacky, A virus.

It's painful and kids hate it, but it's self -limiting.

The key is that posterior location.

It lives in the back of the house.

Contrast that with herpes simplex.

HSV1 usually prefers the anterior mouth, the front of the house.

You'll see vesicles and ulcers on the lips, the gums, we call that gingivostomatitis, and the buccal mucosa, the inside of the cheeks.

It can be incredibly painful.

The gums get bright red and bleed easily.

Then there's candida, the yeast.

Candida doesn't look like an ulcer.

It looks like cottage cheese.

White, curd -like patches stuck to the side of the mouth, the tongue, the palate.

And the diagnostic test for this, it's a physical test, right?

It is, the scrape test.

If you take a tongue blade and scrape off that white patch, and the tissue underneath is red and angry and bleeds, that is candida.

There's one more ulcer type mention that sounds medieval,

vincent angina.

Trench mouth.

It's a fusospirocheteal infection.

It's usually seen in patients with poor oral hygiene.

The gums are necrotic.

There's a gray slough covering ulcers between the teeth.

And the smell.

Putrid.

The text mentions foul breath as a key sign.

If you smell it, you won't forget it.

And finally, the benign one, the canker sore.

Atheistomatitis.

These are the ones we've all had.

Discreet, round ulcers with a yellowish center and a bright red halo.

And where do they show up?

Usually on the inner lip or tongue.

And crucially, no fever, no swollen nodes, just a painful spot.

Okay, that's the ulcer hunt.

Now let's assume there are no ulcers.

We are looking at the tonsils and the pharynx itself.

We are looking for color and exudate.

Redness erythema just tells us inflammation.

It's not specific.

But the exudate, the pus, gives us clues.

The book breaks it down.

Yellow versus white versus gray.

A thick yellowish exudate on the tonsils is often associated with group A strep.

It's not 100%, but it leans that way.

A whiter, thinner exudate is often viral.

And gray.

A thick gray leather -like membrane that covers the tonsils and uvula, that is diphtheria.

Which is exceedingly rare due to vaccines.

Yes, but if you see a gray membrane that bleeds, if you try to peel it off, do not peel it off.

That's the pseudo -membrane of diphtheria, and it's a medical emergency.

Let's talk about strawberry tongue.

I love these food allergies in medicine.

It's a vivid description.

The tongue looks red and bumpy because the papillae are enlarged.

It literally looks like the surface of a strawberry.

And that means?

This is a hallmark of streptococcal infection, specifically scarlet fever.

It comes with that sandpaper rash we'll talk about later.

Now, tonsil size.

We hear tonsils are two plus or three plus.

The text actually defines this in table 32 .1.

It's not just a guess.

It's a standardized scale.

Grade one is visible tonsils just kicking out from behind the pillars.

Grade two is halfway to the uvula.

Grade three is touching the uvula.

Grade four is kissing tonsils.

They're touching in the middle.

They are touching each other in the midline.

The airway is significantly compromised.

And why does this grading matter?

Well, grade four can actually cause airway obstruction like sleep apnea.

But acutely, if you see asymmetry, if one tonsil is a grade three and the other is a grade one, you have to worry.

That points us back to the peritonsillar abscess.

Exactly.

Asymmetry plus a deviated uvula.

The uvula is pushed to the healthy side by the swelling as an abscess until proven otherwise.

Moving down the neck, the lymph nodes.

The text calls this a cardinal sign, but you have to know which nodes to touch.

This is the most common mistake students make.

They just rub the neck vaguely.

You have to distinguish anterior versus posterior.

The anterior cervical chain, where is that?

These went along the front of the sternocleidomastoid muscle.

If these are enlarged and tender, that is highly suggestive of bacterial infection, specifically group A strep.

In the posterior cervical chain, behind the muscle.

If the posterior nodes are swollen, strep is very unlikely.

Posterior adenopathy is the hallmark of viral infections and specifically mononucleosis.

So, front neck hurts,

likely strep.

Back neck hurts, likely mono.

It's a very reliable rule of thumb.

It's one of the best physical exam signs we have for this.

We aren't done with the exam.

The text tells us to look at the nose, the abdomen, and the skin.

Why are we palpating the belly for a sore throat?

We are hunting for the spleen.

Splenomegaly, an enlarged spleen, occurs in about 50 % of mono cases.

And this is a safety issue.

Huge safety issue.

If that spleen is enlarged and the kid goes back to playing football or hockey, a tackle could rupture the spleen.

That is a life -threatening bleed.

You have to feel for it.

And the skin.

We mentioned the sandpaper rash of scarlet fever.

It's a fine red papular rash that feels like sandpaper.

And it spares the palms and soles.

And what about the mono rash?

You also look for a maculopapular rash that can happen with mono, especially if, ironically,

they were mistakenly given amoxicillin for what was thought to be strep.

Right, the amoxicillin rash in mono patients, it turns them bright red.

Exactly.

So the skin tells the story of the throat.

Before we jump to the lab work, we need to cover section five, evidence -based practice.

There is a highlight box in the chapter that specifically deals with managing the peritonsillar abscess we keep talking about.

This is really interesting because it brings some modern technology into the mix.

Historically, diagnosing an abscess was based on that physical exam, the trismus, the deviated uvula.

Right, just looking and feeling.

But the text highlights the use of intraoral ultrasound.

Putting an ultrasound probe inside the mouth.

Exactly.

It sounds tricky, but the sensitivity is incredibly high, 89 to 95%.

It allows you to distinguish between a true abscess, which is a pocket of pus you can drain, and cellulitis, which is just generalized swelling that won't drain.

The text notes it is underused, which implies we should probably be reaching for it more often.

It definitely saves patients from unnecessary needle pokes.

If it's just cellulitis, you don't need to cut it open.

The ultrasound gives you the answer.

Speaking of treatment for the abscess, what's the consensus?

The evidence supports a combination of steroids to reduce the swelling and antibiotics.

Penicillin and metronidazole are listed as effective choices.

And then there's the surgical debate.

Needle aspiration versus incision and drainage.

The poke and drain versus the slice and drain.

The text reviews the literature and finds no clear winner.

So it's dealer's choice.

Pretty much, both are effective.

It usually comes down to provider preference and the size of the abscess.

There's also a note about tonsillectomy.

The old school thought was wait until the infection clears before taking the tonsils out.

Right, the interval tonsillectomy.

But the text points to evidence supporting hot tonsillectomy, taking them out while the abscess is present.

And that's safe.

It turns out it's safe and it actually reduces the total recovery time because you aren't recovering from the abscess and then recovering from surgery months later.

You get it all done at once.

That is a good pearl for the surgical consult.

And generally, can these patients go home?

Surprisingly, yes.

The text says outpatient management is often sufficient as long as, and this is the big caveat, there is no airway compromise.

If they can breathe and swallow their pills, they can often go home.

All right, let's move to section six.

Labs and diagnostics.

We have examined the patient.

We have our suspicion.

Now we need proof.

What is the primary goal of lab testing in a sore throat?

We are back to our main mission.

Identify group A strep to prevent rheumatic fever.

That is the driver.

That's why we swab.

So the rapid strep screen.

This is the test everyone knows.

It's a rapid antigen detection test.

It is fast, which is great.

And it has very high specificity, 95 to 98%.

Let's translate specificity for the students.

High specificity means false positives are rare.

If the test says positive, you can trust it.

The bug is there, you treat.

But the sensitivity is a different story.

Sensitivity is lower, 75 to 85%.

That means if the test says negative, there is still a 15 to 25 % chance the patient actually does have strep.

The test missed it.

So what is the rule?

What does the book say?

The rule is, if positive, treat.

If negative, do not stop.

You must follow up with a throat culture.

The culture is the gold standard.

It is, it takes 24 to 48 hours to grow, but it is the final word.

It catches those cases that a rapid screen missed.

Now let's talk about technique, because the text implies that a lot of false negatives are actually user error.

Oh, absolutely.

The swab technique matters.

You cannot just wave the swab near the mouth.

You have to vigorously swab the tonsils and the posterior pharynx.

You want to get a good sample of that exedit.

And what do you avoid?

You must avoid the tongue and the cheeks.

If you drag the swab across the tongue, you pick up normal oral flora bacteria that live there happily, and you might dilute or contaminate your sample.

It has to be a clean hit on the tonsils.

Let's shift to the mono test.

The monospot.

This test's for heterophyll antibodies.

It's a great test, but it has a major blind spot.

The timing.

Exactly.

Heterophyll antibodies don't appear immediately.

The monospot can be negative in the first one to two weeks of illness.

So if a college student comes in on day three of a sore throat and the monospot is negative.

It means nothing.

They could still have mono.

You have to tell them the test is negative, but you might still have it.

You might need to repeat it in a week or order specific EBV antibody titers, which are more sensitive early on.

Speaking of titers, the text mentions the ASO titer.

I see this ordered inappropriately sometimes.

The ASO antistreptilicin O titer.

The text is very firm on this.

It is not for acute diagnosis.

The ASO titer takes months to rise and peak.

So it tells you about the past, not the present.

Correct.

It is useful if a patient comes in with rheumatic fever, and you want to prove they had strep three weeks ago.

But for the patient sitting in front of you with a sore throat right now, it is useless.

Do not order it.

And finally, imaging.

CT scans.

When do we radiate the neck?

Rarely.

CT is reserved for when you suspect deep mech infections like a retro -pharyngeal abscess, or if you are worried about airway obstruction.

For a standard sore throat, it is overkill.

Okay, we have gathered all our data.

History, exam, labs.

Now we need to synthesize it.

Section seven and eight of the text break down the differential diagnosis based on that big divider we started with.

That's right.

Let's start with section seven.

Pharyngitis without ulcers.

This is the most common bucket.

And the heavyweight champion here is still group A strep.

The text refers to table 32 .2, which is a risk assessment table.

It looks a lot like the center criteria.

It is very similar.

It helped you decide who to test.

It breaks patients into high, medium, and low risk.

What puts someone in the high risk category?

High risk requires a specific combination.

You need the fever, over 101 .5.

You need the anterior cervical adenopathy.

You need the exudate on the tonsils.

And crucially, you need the absence of a cough.

If they have all four.

The probability of strep is very high.

You test, and honestly, some guidelines would say you can treat, but the text emphasizes verifying with testing.

And medium risk.

They have some signs, maybe fever and nodes, but no exudate.

Or maybe exudate and cough.

They're in the middle.

You definitely test before treating.

A low risk.

No fever, likely have a cough.

The probability of strep is so low that the text says, do not test, do not treat.

It is viral.

Reassure them.

The text also drops a truth bomb here.

You cannot diagnose strep by looking alone.

It's true.

50 % of confirmed GIS cases don't look classic.

They might not have the exudate.

They might just look red.

That is why the clinical guesstimate is notoriously inaccurate.

You need the swab.

Let's run through the other new ulcer contenders quickly.

Viral pharyngitis.

The most common.

Sore throat plus cough plus congestion.

The pharynx looks pale or boggy, not fiery red.

You treat with supportive care.

Mononucleosis.

The classic triad.

Fever, sore throat, posterior cervical lymphadenopathy.

Look for that profound fatigue in the splenomegaly.

And on the CBC, look for lymphocytosis.

Specifically, more than 50 % lymphocytes.

Typoglactitis, an abscessor in this category too, technically.

Yes, but they present with those emergency signs, stridor, trismus, that we ruled out in step one.

So they're in their own special bucket.

Gonococcal pharyngitis.

History is key.

Oral sex exposure.

The pharynx might have exudate or might look normal.

You confirm with a specific culture for gonorrhea.

Inflammatory or allergic causes.

Post -nasal drip is the villain here.

The patient will complain of sinus tenderness, no fever, no nodes, just irritation from the drainage running down the back of the throat.

Now, section eight.

Differential diagnosis with ulcers.

We differentiate these by where the ulcers are and what they look like.

Let's do a rapid fire recap.

Let's do it.

Prepagina.

Posterior soft palate.

Summer, fall, kids.

Caused by Coxsackie virus.

Herpes simplex.

Anterior mouth gums, painful vesicles, usually HSV1.

Thins and tangina.

Trench mouth.

Gray necrotic ulcers on the gums.

Foul breath.

Poor hygiene is a risk factor.

Fafthys stomatitis.

Canker sores.

Discrete, round with a red halo.

No fever.

And candidiasis.

White plaques that bleed when scraped.

Not really an ulcer, but a lesion.

Seen in the immunosuppressed or after antibiotic or steroid use.

It is amazing how distinct they are when you lay them out like that.

Location and appearance really tell the story.

It does.

If you stick to the system, checking the location, checking the fever, checking the nodes, the diagnosis usually reveals itself.

So we have walked through the entire chapter.

Let's bring it all together in the outro.

What is the mental roadmap we want our listeners to walk away with?

I think it comes down to a four step process.

Step one, check for the emergency.

Is the airway safe?

Is there drooling, stridor, or trismus?

If yes, stop and refer.

Step two.

Step two, check for ulcers.

Use the big divider.

If yes, categorize by location, anterior versus posterior.

Step three.

If no ulcers, check for strep signs.

Fever plus anterior nodes plus exudate plus no cough.

Use that risk assessment.

And the final step.

Step four, verify.

Use the swab because eyes can be deceiving.

Don't trust your gut alone.

And always, always look beyond the tonsils.

Right.

Palpate the spleen for mono.

Check the skin for rashes for scarlet fever.

Ask about the sexual history for gonorrhea.

The throat is just one part of the patient.

This has been a fascinating deep dive into a topic we see every day.

It really shows that just a sore throat is actually a complex clinical puzzle.

Absolutely.

It's about being systematic, being critical in your thinking, and not skipping steps.

That's how you find the needle in the haystack.

Well, that wraps up our coverage of chapter 32.

We hope you feel ready to tackle the next sore throat that walks through your door with a little more confidence and a lot more precision.

Thanks for listening.

This has been the Last Minute Lecture Team, wishing you a great shift.