October 15, 2025 • 16 mins
Aimed at improving foundational medical knowledge and preparing users for the NBDE Part I exam. The text consists primarily of multiple-choice questions spanning various medical and anatomical topics, including cardiology, neurology, biochemistry, and embryology, each followed by an answer and a detailed explanation. The publisher emphasizes the book's format, which is designed to identify and resolve knowledge deficits, and notes the importance of verifying drug indications and dosages. Furthermore, the material outlines features for quality improvement, such as electronically linked resources for further research and a system for users to flag potential errors or omissions.
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Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Speaker 1 (00:00):
Welcome to the deep dive. You know. We take that
really dense source material, the stuff you just have to know,
and we boil it down give you the essential insights
in a way that hopefully sticks.
Speaker 2 (00:10):
Yeah, and today we're tackling something pretty intense. We're digging
into excerpts from the nbde part I Specialty Review and
self Assessment. This is real foundational stuff, right, and.
Speaker 1 (00:21):
Our goal here is to pull out those high yield facts,
the ones maybe you forget but are actually vital in practice.
Think of it as a detailed shortcut for dental students,
young professionals, anyone needing a solid review.
Speaker 2 (00:34):
And what's interesting about this resource itself, it's not meant
to be your only source of knowledge. It's structured well,
almost like a test. It's designed to pinpoint where your
knowledge gaps are.
Speaker 1 (00:43):
So it makes you confront what you don't know exactly.
Speaker 2 (00:45):
It's like maybe three hundred implied questions woven through it,
and it's peer reviewed constantly, you know, by thousands of professionals.
They even encourage feedback for improvement, which is crucial because
medical science, it never stands still.
Speaker 1 (00:59):
Okay, makes sense, So where do we start with this
mountain of info. How about core cradiofacial anatomy. Those nerve
pathways always trip people up.
Speaker 2 (01:10):
Good starting point. Let's look at the jaw complex, specifically
the medial terygoid muscle. What's really key here isn't just
where it is, but it's nerve supply. It gets innervation
from a branch off the main trunk of V three,
the mandibular division of the trigeminal.
Speaker 1 (01:26):
The main trunk. Okay, why is that specific detail important clinically?
Speaker 2 (01:31):
Well, think about trismus. You know, limited mouth opening. If
you've ruled out the obvious muscle spasm, you have to
consider issues affecting that medial terygoid. Knowing that direct nerve
pathway helps you think about potential injury, maybe even anesthetic
complications affecting that main truck.
Speaker 1 (01:46):
Right, localizing the problem. Yeah, okay, staying in that terygoid area,
let's talk maxillary artery. I remember there are three parts
to it, mandibular, krygoid, and then taragopalatin.
Speaker 2 (01:54):
That's right, And that third part, the tarygo palatine segment,
is really important.
Speaker 1 (01:57):
For why that one specifically.
Speaker 2 (01:59):
Because it's terminal branch the sphenal palatine artery is what
connects things up. It anastomosies or joins with the greater
palatine artery, traveling through the incisive canal.
Speaker 1 (02:11):
Ah. Okay, So that explains the blood supply pathway to
the palate and the nasal septum area precisely.
Speaker 2 (02:18):
It's a critical vascular link for surgery in that region.
Speaker 1 (02:21):
And speaking of critical anatomy, the review mentions the pietarian
Why is that spot so emphasized?
Speaker 2 (02:27):
Yeah, the pietyim that's where anatomy meets well, potentially trauma.
It's structurally the weakest point on the side of the skull.
Speaker 1 (02:34):
Okay, weak point. But what's the immediate danger?
Speaker 2 (02:38):
The danger is what lies directly underneath it. Yeah, the
middle meningeal artery. Remember that's a branch of the maxillary
we just discussed.
Speaker 1 (02:45):
Got it. So a blow to the pietyium.
Speaker 2 (02:46):
Can easily tear that artery, and that leads to an
epidural hematoma, which can build up pressure fast. It's a
true surgical emergency. Weakness plus a major vessel equals high risk.
Speaker 1 (02:56):
Good reminder. Okay, Moving slightly back the TAJ, the review
notes synovial cysts there are rare, but neat surgery, and
also that the terrigoid venus plexus is nearby close to
the lateral terygoid and temporalis muscles.
Speaker 2 (03:12):
Right now, let's switch gears slightly to cranial nerves because
they're so important for diagnosis. Let's focus on CND, the
facial nerve. Distinguishing upper motor neuron versus lower motor neuron
lesions can be tricky.
Speaker 1 (03:24):
Okay, let's break that down. The source points out that
the UMN pathway, the one coming from the brain, has
bilateral innervation for the upper face, right forehead and eye closing.
Speaker 2 (03:33):
Muscles exactly bilateral input to the upper face. So think
about a stroke that's typically a UMN lesion affecting one
side of the brain.
Speaker 1 (03:40):
So the lower face on the opposite side gets paralyzed.
Speaker 2 (03:43):
Correct contralateral lower face paralysis. But because the upper face
muscle still gets signals from the unaffected side of the brain,
forehead movement and eye closing are usually spared.
Speaker 1 (03:53):
Ah Okay, that makes sense. So sparing the forehead points
towards a central UMN problem like a stroke.
Speaker 2 (04:00):
Right now, Contrast that with something like bell palsy that's
an LMN lesion damage directly to the nerve itself or
its nucleus, So the.
Speaker 1 (04:07):
Entire nerve pathway on that side is.
Speaker 2 (04:08):
Out, yes, which means you get paralysis of both the
upper and lower facial muscles. But on the same side
as the nerve damage the ipsilateral side, no forehead wrinkle,
no tied eye closure on that side. That bilateral versus
unilateral innervation is the absolute.
Speaker 1 (04:25):
Key got it? And anatomically, where does see any pop
out of the skull?
Speaker 2 (04:29):
It exits through the stylomustoid formen you find that just
posterior to the styloid process, which itself is the origin
for the stylohyoid muscle. Little landmark connection there.
Speaker 1 (04:38):
Okay, what about CNX The vagus nerve big.
Speaker 2 (04:42):
One, huge, one longest cranial nerve runs down the neck
in the carotid sheath, usually tucked behind the carotid artery
and the internal jugular vein crucial for swallowing because it
innervates the lavator villi palatini.
Speaker 1 (04:53):
The muscle that lists the soft palate.
Speaker 2 (04:55):
Right and nearby you have the tensor velli palatini. Different
innervation though that one's V three. It tenses the soft palette,
but also importantly helps open the eustachian tube when you swallow.
Speaker 1 (05:05):
And if that doesn't work well, like in CLEC Pallette.
Speaker 2 (05:08):
Cases, then you get impure drainage from the middle ear.
That's why those patients often have a higher risk for
otitis media for ear infections. It's a direct mechanical link.
Speaker 1 (05:17):
Wow. Okay, And quickly tying this back to EMBRYOLOGYV. Three,
the mandibular nerve comes from which pharyngeal.
Speaker 2 (05:25):
Arch, that's the first pharyngeal arch, big contributor, also gives
rise to muscles of mastication tensor timpani and that tensor
velli palatine we just mentioned, and systemically remember the third
a order garge develops into the common carotid artery.
Speaker 1 (05:40):
Okay, that's a solid foundation in the head and neck.
Now let's zoom in a bit Section two. Oral structures
and function beyond just chewing right.
Speaker 2 (05:48):
Definitely like the role of teeth, infhonation and speech. It's
something we might not always think about clinically.
Speaker 1 (05:54):
The review highlights the f sound, the if fricative. Why
that specific.
Speaker 2 (05:59):
Sound because making that sound correctly requires the maxillary in
sizors to touch or get very close to the lower lips.
Vermilion border, so.
Speaker 1 (06:08):
Those teeth are missing, or maybe a denture isn't.
Speaker 2 (06:10):
Quite right, the f sound gets distorted. It's a simple
functional check. You can actually hear the problem.
Speaker 1 (06:16):
Interesting and biomechanically. How our teeth built to handle force.
Speaker 2 (06:21):
They're primarily designed for vertical forces, you know, straight down chewing.
The PDL. The periodontal ligament system is amazing at cushioning
and distributing that compressive force to the bone, but.
Speaker 1 (06:32):
They're not great with sideways forces exactly.
Speaker 2 (06:35):
They're weakest against sheer or lateral forces. That's important when
you think about things like grinding, bruxism or checking for mobility.
Speaker 1 (06:43):
Okay, developmental anomalies always cause confusion, gemination versus fusion. How
do we tell them apart? For sure?
Speaker 2 (06:50):
The absolute key is the tooth count. Gemination is like
one tooth bud trying to split into two, so you
get a big, maybe notched crown, But the total number
of teeth in the arch.
Speaker 1 (06:59):
Is normal, Okay, normal count pegemination.
Speaker 2 (07:01):
Right, Fusion is when two separate toothbuds join together during development,
so you end up with one less tooth than normal
on the arch. Just count the teeth that usually gives
you the answer.
Speaker 1 (07:11):
Simple enough, and a quick point on natal teeth. Teeth
babies are born with or get very early.
Speaker 2 (07:18):
Yeah, usually mandibular incisors. They often don't have fully formed roots,
so they can be mobile. Risk of aspiration is one concern.
Another is riga fee disease, basically an ulcer on the
underside of the tongue from rubbing against the tooth. Right.
Speaker 1 (07:31):
Okay, last thing in this section, Yeah, clans parodid versus submandibular.
Speaker 2 (07:36):
Parotic land is almost entirely serious. Secretion thin watery saliva.
It's an ecrin xacrine gland, the submandibular gland, it's SECRETO
motor nerve supply comes from the court to timpany, which
is a branch of CEE NZV and the facial nerve.
See it all connects back.
Speaker 1 (07:52):
It really does. Okay, that sets up the local environment.
Now let's pull back and look at the bigger picture.
Section three, Systemic physiology and metabolism.
Speaker 2 (08:01):
Yeah, you can't isolate the mouth. We need to know
some core physiology like cardiac output CO.
Speaker 1 (08:07):
Remember the formulas CO equals heart rate, time, stroke volume.
Speaker 2 (08:10):
That's one and the other is CO equals map divided
by SVR mean arterial pressure over systemic vascular resistance. Well,
I know both because they show different things affecting output. Say,
under anesthesia, if MAP and heart rate are stable, but
your anesthetic drug causes vasodilation, SVR drops.
Speaker 1 (08:29):
So if SVR goes down, CEO has to go up.
ASSUMINGMAP is constant and stroke volume too.
Speaker 2 (08:35):
Exactly, you need to understand those relationships to manage patients safely.
Speaker 1 (08:38):
Okay, And the lungs have that weird response to hypoxia
right opposite of the rest of the body.
Speaker 2 (08:42):
Yeah, it's sort of counterintuitive. Systemic arterials dilate if oxygen
is low to get more blood flow, but pulmonary arterials
constrict when oxygen is low in that part of the lung.
Speaker 1 (08:52):
Why do they do that.
Speaker 2 (08:53):
It's called hypoxic pulmonary vasoconstriction. It's actually smart. It shunts
blood away from poorly ventilates alveoli towards areas that are
getting good oxygen. It helps match ventilation with perfusion VQ
matching right makes sense.
Speaker 1 (09:07):
Lung volumes FRC functional residual capacity.
Speaker 2 (09:10):
That's the air left in your lungs after you just
breathe out Normally passively. It's the equilibrium point where the
outward pull of the chest wall balances the inward recoil
of the lungs. Mathematically, FRC is erv plus RV expiratory
reserve volume plus residual volume.
Speaker 1 (09:27):
Got it and down at the cell level in the alveoli,
those type two pneumsytes.
Speaker 2 (09:32):
Crucial cells, they make surfactant. That's the stuff that lowers
surface tension inside the alvoli, keeps them from collapsing, especially
during exhalation.
Speaker 1 (09:41):
And if they don't develop properly in infants.
Speaker 2 (09:43):
That's the basis of infant respiratory distress syndrome. No surfactant,
the lungs collapse.
Speaker 1 (09:48):
Okay, let's switch to biochemistry. Gluconeogenesis making new glucose. What
can the body use?
Speaker 2 (09:54):
It can use lactate, certain amino acids, the glycogenic ones,
and glyceryl from.
Speaker 1 (09:59):
Fats, but not fatty acids themselves.
Speaker 2 (10:01):
Correct, fatty acids cannot be directly converted to glucose. And
a detail about glycerol. You actually need two molecules of
glycerool to make one molecule of glucose.
Speaker 1 (10:11):
Good detail vitamin deficiencies. The review mentions biotin B seven
the raw egg white connection.
Speaker 2 (10:17):
Yeah, raw egg whites contain avidin, a protein that binds
biotin really tightly and prevents its absorption. Eat enough raw
eggs you could theoretically induce a biotin deficiency affecting metabolism.
Speaker 1 (10:27):
And there's a link between reboflaviin B two and niosin
B three.
Speaker 2 (10:31):
Yes, riboflavon deficiency can actually mess up niosin metabolism. You
need riboflaviin cofactors to make nad and nadp from tryp
to fan, which is a precursor for niosin. So low
B two could indirectly lead to symptoms resembling pelagra, the
niosin deficiency disease.
Speaker 1 (10:48):
Hmm, interesting cascade. What about minerals high zinc intake causing problems?
Speaker 2 (10:53):
Yeah, this is a clinically relevant one. Taking high doses
of zinc supplements long term can lead to a copper deficiency.
Speaker 1 (11:00):
How does that happen?
Speaker 2 (11:01):
It involves a protein in the intestinal cells called metallithiamine.
High zinc levels make the gut cells produce more of it.
This protein binds copper even more strongly than zinc, basically
trapping the dietary copper inside the intestinal cells, so it
can't be absorbed.
Speaker 1 (11:16):
Wow. Okay. Endocrine system points.
Speaker 2 (11:18):
Glucotinase found in the pancreas and liver. It acts like
a glucose sensor. Really, it gets activated when glucose levels
are high and in the pancreas this triggers insulin release.
Speaker 1 (11:27):
And prolactin what controls its release.
Speaker 2 (11:29):
It's mainly under inhibitory control by dopamine from the hypothalamus.
Think of dopamine as a break remove the brake and
prolactin levels go up.
Speaker 1 (11:37):
Okay, And cortisol. The glucocorticoids, how do they work.
Speaker 2 (11:41):
They act via intracellular receptors. They go into the cell,
bind to receptors and then influence gene transcription. That's why
they have such widespread effects on metabolism the immune system
and cause things like skin thinning or muscle breakdown with
chronic exposure.
Speaker 1 (11:56):
Right affecting protein synthesism breakdown. Okay, that covers the big systems.
Last section, histology, pathology and wound repair. Skin layers first,
where do they come from?
Speaker 2 (12:06):
Embryonically pre straightforward dermis. The deeper layer is from mesoderme epidermis.
The outer layer is from surface ectoderm, but melanocytes the
pigment cells, they have a different origin neural crust.
Speaker 1 (12:19):
Okay. Wound healing phases are critical. When does that grainy
red tissue granulation tissue show.
Speaker 2 (12:25):
Up that starts forming in the proliferative phase, typically around
days three to five after injury.
Speaker 1 (12:30):
And the wound actually shrinking contracting.
Speaker 2 (12:32):
That's mainly driven by myofibroblasts. These specialized cells appear a
bit later, maybe starting around a week one, and they
actively pull the wound edges together. You can identify them
by their expression of alpha smooth muscle actin.
Speaker 1 (12:45):
And the final longest phase, remodeling.
Speaker 2 (12:48):
Yeah, the maturation or remodeling phase starts around week three
or four, but can take a year or even more.
Key players here are macrophases, which release growth factors like EGF.
This stimulates fibroblasts to produce collagenase enzymes, which break down
and reorganize the initial weaker collagen into a stronger scar.
Speaker 1 (13:07):
Makes sense. Right at the very start of an injury,
who's the first cell to arrive on the scene.
Speaker 2 (13:12):
That's the neutrophil, the first responder. Histologically, you'd see them
as cells with multilobed nuclei and cytoplasm that looks kind
of pinkish. Eosanophilic with fine granules, okay.
Speaker 1 (13:22):
Imminopithology anaphylaxis classic type I hypersensitivity.
Speaker 2 (13:27):
It's mediated by IgE antibodies binding to mass cells, causing
them to degranulate and release histamine and other mediators. Clinically,
measuring trip tase levels can help confirm that mass cell
degranulation occurred.
Speaker 1 (13:38):
GOT and chronic grandulomitis disease CGD.
Speaker 2 (13:41):
That's an immune deficiency. The problem is a defect in
the nadph oxidase enzyme. This enzyme normally produces superoxide radicals,
which neutrophils use to kill bacteria they've ingested. Without it,
patients get recurrent infections, especially from catalyse positive organisms like
Staph aureus, because they can break down the little bit
(14:01):
of peroxide.
Speaker 1 (14:02):
The cell might make right, they can protect themselves. And finally,
a cancer sign in histology nuclear hypochromasia.
Speaker 2 (14:10):
Yeah. When you look at malignant cells under the microscope,
particularly in high grade tumors like some bladder cancers, the
nuclei often appear very dark and irregularly clumped. That's hyperchromasia,
increased sustaining due to more DNA and clumped chromatin. It's
a sign of anaplasia, that loss of normal cell features.
Speaker 1 (14:27):
Okay, that was definitely a deep dive through a lot
of core material.
Speaker 2 (14:30):
It really shows how interconnected everything is, doesn't It From
a specific nerve branch and the jaw all the way
to how glucose is made or how wounds heal.
Speaker 1 (14:38):
Absolutely and the So what for you listening, especially if
you're starting out, is that knowing these fundamentals helps you
connect the dots. You see something in the mouth, maybe
an odd finding or a sign of deficiency, and this
knowledge helps you think about potential underlying systemic issues. It's
foundational for truly comprehensive care.
Speaker 2 (14:55):
Right. So to help block some of this in, let's
do a quick review question. Think about this anatomically. Where
exactly is the opening the orifice of the coronary sinus
located and what's its clinical significance?
Speaker 1 (15:08):
Okay, the location it's in the right atrium. You'd find
it medial to the opening of the inferior venaicava the
IVC and just superior to the septal leaflet of the
tricuspid valve and it's significant. Well, it's the main vein
draining the heart muscle itself, the myocardium, and clinically, the
muscle sleeve around its opening can sometimes be a source
of abnormal electrical activity atopic beats, so it's often a
(15:30):
target area during electrophysiology procedures like ablations for Arristhmius nicely summarized.
Speaker 2 (15:36):
Okay, one final provocative thought to leave you with. We
learn anatomy from textbooks, often presented as fixed, but the
real world has variations. For example, the bovine arch, where
the brachiocephalic trunk gives rise to three arteries instead of
the usual two, occurs in something like fourteen percent of people.
That's quite common, it is, So the question is how
does knowing that common anatomical variations like this exist, maybe
(16:00):
an unusual nerve path or an extra blood vessel. How
does that affect your clinical certainty when you're looking at
an X ray or diagnosing a problem? How do you
factor in that possibility variation? Something to think about until
our next deep dive
Welcome to the deep dive. You know. We take that
really dense source material, the stuff you just have to know,
and we boil it down give you the essential insights
in a way that hopefully sticks.
Speaker 2 (00:10):
Yeah, and today we're tackling something pretty intense. We're digging
into excerpts from the nbde part I Specialty Review and
self Assessment. This is real foundational stuff, right, and.
Speaker 1 (00:21):
Our goal here is to pull out those high yield facts,
the ones maybe you forget but are actually vital in practice.
Think of it as a detailed shortcut for dental students,
young professionals, anyone needing a solid review.
Speaker 2 (00:34):
And what's interesting about this resource itself, it's not meant
to be your only source of knowledge. It's structured well,
almost like a test. It's designed to pinpoint where your
knowledge gaps are.
Speaker 1 (00:43):
So it makes you confront what you don't know exactly.
Speaker 2 (00:45):
It's like maybe three hundred implied questions woven through it,
and it's peer reviewed constantly, you know, by thousands of professionals.
They even encourage feedback for improvement, which is crucial because
medical science, it never stands still.
Speaker 1 (00:59):
Okay, makes sense, So where do we start with this
mountain of info. How about core cradiofacial anatomy. Those nerve
pathways always trip people up.
Speaker 2 (01:10):
Good starting point. Let's look at the jaw complex, specifically
the medial terygoid muscle. What's really key here isn't just
where it is, but it's nerve supply. It gets innervation
from a branch off the main trunk of V three,
the mandibular division of the trigeminal.
Speaker 1 (01:26):
The main trunk. Okay, why is that specific detail important clinically?
Speaker 2 (01:31):
Well, think about trismus. You know, limited mouth opening. If
you've ruled out the obvious muscle spasm, you have to
consider issues affecting that medial terygoid. Knowing that direct nerve
pathway helps you think about potential injury, maybe even anesthetic
complications affecting that main truck.
Speaker 1 (01:46):
Right, localizing the problem. Yeah, okay, staying in that terygoid area,
let's talk maxillary artery. I remember there are three parts
to it, mandibular, krygoid, and then taragopalatin.
Speaker 2 (01:54):
That's right, And that third part, the tarygo palatine segment,
is really important.
Speaker 1 (01:57):
For why that one specifically.
Speaker 2 (01:59):
Because it's terminal branch the sphenal palatine artery is what
connects things up. It anastomosies or joins with the greater
palatine artery, traveling through the incisive canal.
Speaker 1 (02:11):
Ah. Okay, So that explains the blood supply pathway to
the palate and the nasal septum area precisely.
Speaker 2 (02:18):
It's a critical vascular link for surgery in that region.
Speaker 1 (02:21):
And speaking of critical anatomy, the review mentions the pietarian
Why is that spot so emphasized?
Speaker 2 (02:27):
Yeah, the pietyim that's where anatomy meets well, potentially trauma.
It's structurally the weakest point on the side of the skull.
Speaker 1 (02:34):
Okay, weak point. But what's the immediate danger?
Speaker 2 (02:38):
The danger is what lies directly underneath it. Yeah, the
middle meningeal artery. Remember that's a branch of the maxillary
we just discussed.
Speaker 1 (02:45):
Got it. So a blow to the pietyium.
Speaker 2 (02:46):
Can easily tear that artery, and that leads to an
epidural hematoma, which can build up pressure fast. It's a
true surgical emergency. Weakness plus a major vessel equals high risk.
Speaker 1 (02:56):
Good reminder. Okay, Moving slightly back the TAJ, the review
notes synovial cysts there are rare, but neat surgery, and
also that the terrigoid venus plexus is nearby close to
the lateral terygoid and temporalis muscles.
Speaker 2 (03:12):
Right now, let's switch gears slightly to cranial nerves because
they're so important for diagnosis. Let's focus on CND, the
facial nerve. Distinguishing upper motor neuron versus lower motor neuron
lesions can be tricky.
Speaker 1 (03:24):
Okay, let's break that down. The source points out that
the UMN pathway, the one coming from the brain, has
bilateral innervation for the upper face, right forehead and eye closing.
Speaker 2 (03:33):
Muscles exactly bilateral input to the upper face. So think
about a stroke that's typically a UMN lesion affecting one
side of the brain.
Speaker 1 (03:40):
So the lower face on the opposite side gets paralyzed.
Speaker 2 (03:43):
Correct contralateral lower face paralysis. But because the upper face
muscle still gets signals from the unaffected side of the brain,
forehead movement and eye closing are usually spared.
Speaker 1 (03:53):
Ah Okay, that makes sense. So sparing the forehead points
towards a central UMN problem like a stroke.
Speaker 2 (04:00):
Right now, Contrast that with something like bell palsy that's
an LMN lesion damage directly to the nerve itself or
its nucleus, So the.
Speaker 1 (04:07):
Entire nerve pathway on that side is.
Speaker 2 (04:08):
Out, yes, which means you get paralysis of both the
upper and lower facial muscles. But on the same side
as the nerve damage the ipsilateral side, no forehead wrinkle,
no tied eye closure on that side. That bilateral versus
unilateral innervation is the absolute.
Speaker 1 (04:25):
Key got it? And anatomically, where does see any pop
out of the skull?
Speaker 2 (04:29):
It exits through the stylomustoid formen you find that just
posterior to the styloid process, which itself is the origin
for the stylohyoid muscle. Little landmark connection there.
Speaker 1 (04:38):
Okay, what about CNX The vagus nerve big.
Speaker 2 (04:42):
One, huge, one longest cranial nerve runs down the neck
in the carotid sheath, usually tucked behind the carotid artery
and the internal jugular vein crucial for swallowing because it
innervates the lavator villi palatini.
Speaker 1 (04:53):
The muscle that lists the soft palate.
Speaker 2 (04:55):
Right and nearby you have the tensor velli palatini. Different
innervation though that one's V three. It tenses the soft palette,
but also importantly helps open the eustachian tube when you swallow.
Speaker 1 (05:05):
And if that doesn't work well, like in CLEC Pallette.
Speaker 2 (05:08):
Cases, then you get impure drainage from the middle ear.
That's why those patients often have a higher risk for
otitis media for ear infections. It's a direct mechanical link.
Speaker 1 (05:17):
Wow. Okay, And quickly tying this back to EMBRYOLOGYV. Three,
the mandibular nerve comes from which pharyngeal.
Speaker 2 (05:25):
Arch, that's the first pharyngeal arch, big contributor, also gives
rise to muscles of mastication tensor timpani and that tensor
velli palatine we just mentioned, and systemically remember the third
a order garge develops into the common carotid artery.
Speaker 1 (05:40):
Okay, that's a solid foundation in the head and neck.
Now let's zoom in a bit Section two. Oral structures
and function beyond just chewing right.
Speaker 2 (05:48):
Definitely like the role of teeth, infhonation and speech. It's
something we might not always think about clinically.
Speaker 1 (05:54):
The review highlights the f sound, the if fricative. Why
that specific.
Speaker 2 (05:59):
Sound because making that sound correctly requires the maxillary in
sizors to touch or get very close to the lower lips.
Vermilion border, so.
Speaker 1 (06:08):
Those teeth are missing, or maybe a denture isn't.
Speaker 2 (06:10):
Quite right, the f sound gets distorted. It's a simple
functional check. You can actually hear the problem.
Speaker 1 (06:16):
Interesting and biomechanically. How our teeth built to handle force.
Speaker 2 (06:21):
They're primarily designed for vertical forces, you know, straight down chewing.
The PDL. The periodontal ligament system is amazing at cushioning
and distributing that compressive force to the bone, but.
Speaker 1 (06:32):
They're not great with sideways forces exactly.
Speaker 2 (06:35):
They're weakest against sheer or lateral forces. That's important when
you think about things like grinding, bruxism or checking for mobility.
Speaker 1 (06:43):
Okay, developmental anomalies always cause confusion, gemination versus fusion. How
do we tell them apart? For sure?
Speaker 2 (06:50):
The absolute key is the tooth count. Gemination is like
one tooth bud trying to split into two, so you
get a big, maybe notched crown, But the total number
of teeth in the arch.
Speaker 1 (06:59):
Is normal, Okay, normal count pegemination.
Speaker 2 (07:01):
Right, Fusion is when two separate toothbuds join together during development,
so you end up with one less tooth than normal
on the arch. Just count the teeth that usually gives
you the answer.
Speaker 1 (07:11):
Simple enough, and a quick point on natal teeth. Teeth
babies are born with or get very early.
Speaker 2 (07:18):
Yeah, usually mandibular incisors. They often don't have fully formed roots,
so they can be mobile. Risk of aspiration is one concern.
Another is riga fee disease, basically an ulcer on the
underside of the tongue from rubbing against the tooth. Right.
Speaker 1 (07:31):
Okay, last thing in this section, Yeah, clans parodid versus submandibular.
Speaker 2 (07:36):
Parotic land is almost entirely serious. Secretion thin watery saliva.
It's an ecrin xacrine gland, the submandibular gland, it's SECRETO
motor nerve supply comes from the court to timpany, which
is a branch of CEE NZV and the facial nerve.
See it all connects back.
Speaker 1 (07:52):
It really does. Okay, that sets up the local environment.
Now let's pull back and look at the bigger picture.
Section three, Systemic physiology and metabolism.
Speaker 2 (08:01):
Yeah, you can't isolate the mouth. We need to know
some core physiology like cardiac output CO.
Speaker 1 (08:07):
Remember the formulas CO equals heart rate, time, stroke volume.
Speaker 2 (08:10):
That's one and the other is CO equals map divided
by SVR mean arterial pressure over systemic vascular resistance. Well,
I know both because they show different things affecting output. Say,
under anesthesia, if MAP and heart rate are stable, but
your anesthetic drug causes vasodilation, SVR drops.
Speaker 1 (08:29):
So if SVR goes down, CEO has to go up.
ASSUMINGMAP is constant and stroke volume too.
Speaker 2 (08:35):
Exactly, you need to understand those relationships to manage patients safely.
Speaker 1 (08:38):
Okay, And the lungs have that weird response to hypoxia
right opposite of the rest of the body.
Speaker 2 (08:42):
Yeah, it's sort of counterintuitive. Systemic arterials dilate if oxygen
is low to get more blood flow, but pulmonary arterials
constrict when oxygen is low in that part of the lung.
Speaker 1 (08:52):
Why do they do that.
Speaker 2 (08:53):
It's called hypoxic pulmonary vasoconstriction. It's actually smart. It shunts
blood away from poorly ventilates alveoli towards areas that are
getting good oxygen. It helps match ventilation with perfusion VQ
matching right makes sense.
Speaker 1 (09:07):
Lung volumes FRC functional residual capacity.
Speaker 2 (09:10):
That's the air left in your lungs after you just
breathe out Normally passively. It's the equilibrium point where the
outward pull of the chest wall balances the inward recoil
of the lungs. Mathematically, FRC is erv plus RV expiratory
reserve volume plus residual volume.
Speaker 1 (09:27):
Got it and down at the cell level in the alveoli,
those type two pneumsytes.
Speaker 2 (09:32):
Crucial cells, they make surfactant. That's the stuff that lowers
surface tension inside the alvoli, keeps them from collapsing, especially
during exhalation.
Speaker 1 (09:41):
And if they don't develop properly in infants.
Speaker 2 (09:43):
That's the basis of infant respiratory distress syndrome. No surfactant,
the lungs collapse.
Speaker 1 (09:48):
Okay, let's switch to biochemistry. Gluconeogenesis making new glucose. What
can the body use?
Speaker 2 (09:54):
It can use lactate, certain amino acids, the glycogenic ones,
and glyceryl from.
Speaker 1 (09:59):
Fats, but not fatty acids themselves.
Speaker 2 (10:01):
Correct, fatty acids cannot be directly converted to glucose. And
a detail about glycerol. You actually need two molecules of
glycerool to make one molecule of glucose.
Speaker 1 (10:11):
Good detail vitamin deficiencies. The review mentions biotin B seven
the raw egg white connection.
Speaker 2 (10:17):
Yeah, raw egg whites contain avidin, a protein that binds
biotin really tightly and prevents its absorption. Eat enough raw
eggs you could theoretically induce a biotin deficiency affecting metabolism.
Speaker 1 (10:27):
And there's a link between reboflaviin B two and niosin
B three.
Speaker 2 (10:31):
Yes, riboflavon deficiency can actually mess up niosin metabolism. You
need riboflaviin cofactors to make nad and nadp from tryp
to fan, which is a precursor for niosin. So low
B two could indirectly lead to symptoms resembling pelagra, the
niosin deficiency disease.
Speaker 1 (10:48):
Hmm, interesting cascade. What about minerals high zinc intake causing problems?
Speaker 2 (10:53):
Yeah, this is a clinically relevant one. Taking high doses
of zinc supplements long term can lead to a copper deficiency.
Speaker 1 (11:00):
How does that happen?
Speaker 2 (11:01):
It involves a protein in the intestinal cells called metallithiamine.
High zinc levels make the gut cells produce more of it.
This protein binds copper even more strongly than zinc, basically
trapping the dietary copper inside the intestinal cells, so it
can't be absorbed.
Speaker 1 (11:16):
Wow. Okay. Endocrine system points.
Speaker 2 (11:18):
Glucotinase found in the pancreas and liver. It acts like
a glucose sensor. Really, it gets activated when glucose levels
are high and in the pancreas this triggers insulin release.
Speaker 1 (11:27):
And prolactin what controls its release.
Speaker 2 (11:29):
It's mainly under inhibitory control by dopamine from the hypothalamus.
Think of dopamine as a break remove the brake and
prolactin levels go up.
Speaker 1 (11:37):
Okay, And cortisol. The glucocorticoids, how do they work.
Speaker 2 (11:41):
They act via intracellular receptors. They go into the cell,
bind to receptors and then influence gene transcription. That's why
they have such widespread effects on metabolism the immune system
and cause things like skin thinning or muscle breakdown with
chronic exposure.
Speaker 1 (11:56):
Right affecting protein synthesism breakdown. Okay, that covers the big systems.
Last section, histology, pathology and wound repair. Skin layers first,
where do they come from?
Speaker 2 (12:06):
Embryonically pre straightforward dermis. The deeper layer is from mesoderme epidermis.
The outer layer is from surface ectoderm, but melanocytes the
pigment cells, they have a different origin neural crust.
Speaker 1 (12:19):
Okay. Wound healing phases are critical. When does that grainy
red tissue granulation tissue show.
Speaker 2 (12:25):
Up that starts forming in the proliferative phase, typically around
days three to five after injury.
Speaker 1 (12:30):
And the wound actually shrinking contracting.
Speaker 2 (12:32):
That's mainly driven by myofibroblasts. These specialized cells appear a
bit later, maybe starting around a week one, and they
actively pull the wound edges together. You can identify them
by their expression of alpha smooth muscle actin.
Speaker 1 (12:45):
And the final longest phase, remodeling.
Speaker 2 (12:48):
Yeah, the maturation or remodeling phase starts around week three
or four, but can take a year or even more.
Key players here are macrophases, which release growth factors like EGF.
This stimulates fibroblasts to produce collagenase enzymes, which break down
and reorganize the initial weaker collagen into a stronger scar.
Speaker 1 (13:07):
Makes sense. Right at the very start of an injury,
who's the first cell to arrive on the scene.
Speaker 2 (13:12):
That's the neutrophil, the first responder. Histologically, you'd see them
as cells with multilobed nuclei and cytoplasm that looks kind
of pinkish. Eosanophilic with fine granules, okay.
Speaker 1 (13:22):
Imminopithology anaphylaxis classic type I hypersensitivity.
Speaker 2 (13:27):
It's mediated by IgE antibodies binding to mass cells, causing
them to degranulate and release histamine and other mediators. Clinically,
measuring trip tase levels can help confirm that mass cell
degranulation occurred.
Speaker 1 (13:38):
GOT and chronic grandulomitis disease CGD.
Speaker 2 (13:41):
That's an immune deficiency. The problem is a defect in
the nadph oxidase enzyme. This enzyme normally produces superoxide radicals,
which neutrophils use to kill bacteria they've ingested. Without it,
patients get recurrent infections, especially from catalyse positive organisms like
Staph aureus, because they can break down the little bit
(14:01):
of peroxide.
Speaker 1 (14:02):
The cell might make right, they can protect themselves. And finally,
a cancer sign in histology nuclear hypochromasia.
Speaker 2 (14:10):
Yeah. When you look at malignant cells under the microscope,
particularly in high grade tumors like some bladder cancers, the
nuclei often appear very dark and irregularly clumped. That's hyperchromasia,
increased sustaining due to more DNA and clumped chromatin. It's
a sign of anaplasia, that loss of normal cell features.
Speaker 1 (14:27):
Okay, that was definitely a deep dive through a lot
of core material.
Speaker 2 (14:30):
It really shows how interconnected everything is, doesn't It From
a specific nerve branch and the jaw all the way
to how glucose is made or how wounds heal.
Speaker 1 (14:38):
Absolutely and the So what for you listening, especially if
you're starting out, is that knowing these fundamentals helps you
connect the dots. You see something in the mouth, maybe
an odd finding or a sign of deficiency, and this
knowledge helps you think about potential underlying systemic issues. It's
foundational for truly comprehensive care.
Speaker 2 (14:55):
Right. So to help block some of this in, let's
do a quick review question. Think about this anatomically. Where
exactly is the opening the orifice of the coronary sinus
located and what's its clinical significance?
Speaker 1 (15:08):
Okay, the location it's in the right atrium. You'd find
it medial to the opening of the inferior venaicava the
IVC and just superior to the septal leaflet of the
tricuspid valve and it's significant. Well, it's the main vein
draining the heart muscle itself, the myocardium, and clinically, the
muscle sleeve around its opening can sometimes be a source
of abnormal electrical activity atopic beats, so it's often a
(15:30):
target area during electrophysiology procedures like ablations for Arristhmius nicely summarized.
Speaker 2 (15:36):
Okay, one final provocative thought to leave you with. We
learn anatomy from textbooks, often presented as fixed, but the
real world has variations. For example, the bovine arch, where
the brachiocephalic trunk gives rise to three arteries instead of
the usual two, occurs in something like fourteen percent of people.
That's quite common, it is, So the question is how
does knowing that common anatomical variations like this exist, maybe
(16:00):
an unusual nerve path or an extra blood vessel. How
does that affect your clinical certainty when you're looking at
an X ray or diagnosing a problem? How do you
factor in that possibility variation? Something to think about until
our next deep dive
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