Speaker 1: You know, usually when we look at a dental diagnosis,
Speaker 1: there's this expectation of clinical precision.
Speaker 2: Right like an engineering mindset.
Speaker 1: Exactly like a patient comes in with a fractured cusp,
Speaker 1: the radiograph shows that jagged white line and you point
Speaker 1: to it on the monitor and say, well, there it is.
Speaker 1: That's the structural failure. It's clean, it's isolated, and honestly
Speaker 1: it's comforting.
Speaker 2: It creates an illusion of control. Really. I mean, we're
Speaker 2: trained to operate in millimeters, focusing so intensely on the
Speaker 2: hard tissues in the immediate periodontium. But the reality of
Speaker 2: otter and clinical practice is just far less isolated.
Speaker 1: Yeah, because then you look down at the patient's medical
Speaker 1: history form and that neat structural mindset just completely shatters.
Speaker 2: It really does.
Speaker 1: Suddenly you aren't just treating a fractured tooth or you know,
Speaker 1: a coufurious lesion. You're operating inside this highly complex systemic
Speaker 1: environment that has been fundamentally re engineered by prescription drugs.
Speaker 1: And for you listening to this deep dive as a
Speaker 1: dental student or young professional, navigating that pharmacological landscape is
Speaker 1: quite literally the difference between a routine procedure and a
Speaker 1: life threatening medical emergency.
Speaker 2: Absolutely, And that's exactly why the Drug Dictionary for Dentistry
Speaker 2: by Mitchen and Seymour is so vital. It establishes a
Speaker 2: core philosophy for this exact reality. Right.
Speaker 1: Our mission today is to pull the real world clinical
Speaker 1: pearls from this guide, right, not just read a list.
Speaker 2: Yeah, we have to move beyond just memorizing alphabetical lists
Speaker 2: of side effects. I mean, a patient's medical history isn't
Speaker 2: just a background check. It's the ultimate, non negotiable blueprint
Speaker 2: for their dental treatment plan. We need to understand the
Speaker 2: underlying physiological mechanisms, like the why and the how, because
Speaker 2: that is what dictates clinical management.
Speaker 1: So we're going to break this down into four clinical
Speaker 1: pillars today. Let's start with the immediate oral environment. When
Speaker 1: a patient opens their mouth, before you even pick up
Speaker 1: an explorer, you're often looking at a chemically altered landscape. Oh,
Speaker 1: like we see zerostomia constantly. But we need to look
Speaker 1: past the obvious discomfort. You know, saliva isn't just lubrication.
Speaker 1: I always compare a mouth without saliva to a car
Speaker 1: engine running without oil. You get friction, decay, and eventual breakdown.
Speaker 1: It's a continuous buffering liquid immune system.
Speaker 2: That's a great analogy. Yeah, and when that salivary flow
Speaker 2: is suppressed, you are stripping away the primary defense mechanism
Speaker 2: against demineralization and opportunistic pathogens. The text emphasizes how ubiquitous
Speaker 2: this parasympathetic inhibition is across vastly different pharmacological classes. I mean,
Speaker 2: you see severe salivary flow reduction with tricyclic antidepressants like
Speaker 2: amatrypti line in disulibin, which are so calmon very common,
Speaker 2: and antipsychotics like amazyl pride and quishiapine, and histamines like acrovastine,
Speaker 2: even asima medications like amtophyline. They all disrupt the autonomic
Speaker 2: pathways that stimulate the salivary glands.
Speaker 1: So the buffering capacity plummets, the oral pH drocks and
Speaker 1: you get this massive carryogenic shift. Clinically, if that patient
Speaker 1: is dentate, you can't just suggest they rank a little
Speaker 1: more water.
Speaker 2: No, definitely not.
Speaker 1: They require an immediate, aggressive, high carries risk protocol, so
Speaker 1: prescription topical fluorides, remineralizing pastes, artificial saliva, and for addentialist patients,
Speaker 1: the prosodonic implications are just disastrous.
Speaker 2: Oh, it ruins the retention.
Speaker 1: Yeah, you lose that crucial microscopic layer of saliva, which
Speaker 1: means you lose the surface tension and capillary action required
Speaker 1: for denture attention. The acrylic just won't seal to the mucosa.
Speaker 2: It destabilizes the entire restorative foundation. And while salvary suppression
Speaker 2: alters the biochemical environment, other systemic drugs are aggressively altering
Speaker 2: the physical architecture of the hard and soft tissues.
Speaker 1: Like gingibal overgrowth.
Speaker 2: Exactly. We learn early on about fennytoin and gingibal overgrowth,
Speaker 2: which is driven by an alteration in fibroblast metabolism, but
Speaker 2: the dictionary highlights far more insidious structural defects caused by
Speaker 2: this anti convulsant.
Speaker 1: Wait, like what the root architecture changes?
Speaker 2: Right? It does. Yeah, finnytoin is associated with severe root shortening,
Speaker 2: root resorption, and hyper semintosis. You get this massive excessive
Speaker 2: deposition of cementum along the apical third of the roots.
Speaker 1: Wow, Okay, so clinically that's a nightmare for extractions.
Speaker 2: Right, if you're planning an extraction on a patient with
Speaker 2: a long history of fennytoyin use. What looks like a straightforward,
Speaker 2: simple elevation on the radiograph will often turn into a
Speaker 2: brutal surgical extraction because that hyper seminosis essentially anchors the
Speaker 2: tooth into the alveolar bone like a rivet.
Speaker 1: That's crazy to think about.
Speaker 2: And additionally, for female patients of child bearing age, finny
Speaker 2: toyin carries a heavily documented to ratogenic risk for cleft,
Speaker 2: lip and palate.
Speaker 1: Right, and we also see significant tissue alterations with calcium
Speaker 1: channel blockers too, don't we.
Speaker 2: Yeah, Drugs like is ratifine and then sold to pain they.
Speaker 1: Interfere with intracellular calcium mobilization, which somehow triggers that same
Speaker 1: pronounced anterior gingibal overgrowth, completely complicating oral hygiene and periodonal maintenance.
Speaker 2: It's a very visible side effect.
Speaker 1: But let's look at it much more acute volatile tissue
Speaker 1: reaction angioedema the sudden massive swelling of the lips, tongue,
Speaker 1: and the floor of the mouth. The text flags ace
Speaker 1: inhibitors like solazeprol and bisphosphonse like allandronic acid as primary triggers.
Speaker 2: Yes, this is a critical one.
Speaker 1: Now in a high stress scenario. If a patient's tongue
Speaker 1: starts swelling rapidly in the chair, instinct dictates grabbing the
Speaker 1: emergency kit, hitting them with an EpiPen, and falling up
Speaker 1: with hedrochurtisome. But the literature suggests that's a trap. Right.
Speaker 1: Why does standard anaphylaxis protocol fail here?
Speaker 2: Because the mechanism of action is fundamentally different from a
Speaker 2: type bi hypersensitivity reaction. Oh so, if a patient is
Speaker 2: allergic to penicillin, you have an IgE mediated response causing
Speaker 2: mass cells to degranulate and release massive amounts of histamine.
Speaker 1: Right, and that's where the epinephrin comes in.
Speaker 2: Exactly. Epinephrine and corticosteroids aggressively target and reverse that histamine pathway.
Speaker 2: But ace inhibitor induced angioedema is not mediator by histamin Oh. Interesting, Yeah,
Speaker 2: ace engie intents and converting enzyme is also responsible for
Speaker 2: breaking down bradikeinan, which is a potent endogenous phasodilator. When
Speaker 2: you inhibit ace, brite akeenin accumulates in the tissues, leading
Speaker 2: to massive fluid extravasation and swelling.
Speaker 1: So hitting them with epinephrine does absolutely nothing for the
Speaker 1: brandikeine accumulation.
Speaker 2: It is functionally useless in this specific pathway, the swelling
Speaker 2: will just continue despite the adrenaline. Wow. This is why
Speaker 2: you must proactively question patients on ace inhibitors about any
Speaker 2: history of transient swelling, swallowing difficulties, or airway embarrassment before
Speaker 2: initiating treatment. Even minor dental trauma or local anesthetic injections
Speaker 2: can precipitate this bratikin and mediated crisis.
Speaker 1: Okay, so we've got mucosal swelling, structural changes, and salivary collapse.
Speaker 1: But let's pivot. That's just the surface level, right, that's
Speaker 1: what we can see. Yeah, if you're planning any sort
Speaker 1: of invasive procedure and extraction, implant placement, or pyioflap surgery,
Speaker 1: the real threat is what's happening beneath the mucosa in
Speaker 1: the blood and bone.
Speaker 2: The hemenotological environment literally dictates your surgical success or failure.
Speaker 2: The dictionary establishes a rigid clinical threshold here, it's the
Speaker 2: less than one hundred thousand platelet rule.
Speaker 1: Right, Because we're looking at a massive spectrum of drugs
Speaker 1: that induce bone marrow suppression. Chemotherapeutic agents like eclarubasin and
Speaker 1: carboplatin are expected obviously sure, but the list extends to
Speaker 1: rheumatology drugs like penicillamine and psychiatric medications like maprobamate. They
Speaker 1: trigger profound frombocyopenia, a granular of cytosis and lekopenia.
Speaker 2: And you know, the physiology of hemostasis relies heavily on
Speaker 2: that initial platelet plug to form the scaffold for the
Speaker 2: coagulation cascade. Once a patient's platelet count drops below one
Speaker 2: hundred thousand per micro leader, normal physiological clotting mechanisms become
Speaker 2: fundamentally inadequate.
Speaker 1: For dental surgery, a routine extraction site will simply not
Speaker 1: stop oozing exactly.
Speaker 2: You have to step in and artificially manufacture hemostasis. You
Speaker 2: can't just place a cotton roll and rely on pressure.
Speaker 1: So what do you do?
Speaker 2: You need to actively pack the socket with oxidized, regenerated
Speaker 2: cellulose or gelatin sponges, place Figure eight tension sutures to
Speaker 2: physically approximate the tissue, and have the logistical groundwork laid
Speaker 2: to request an immediate plately transfusion if refractory bleeding occurs.
Speaker 1: Right, and that bone marrow suppression isn't just about platelets.
Speaker 1: We also mention a granular cytosis.
Speaker 2: Yeah, stripping away the granular lecocytes, the NEUTROPHILSI, asenophils, and
Speaker 2: basophyls means the patient has lost their cellular first responders.
Speaker 1: So clinically, what does that look like?
Speaker 2: Clinically? This manifests as a staggering susceptibility to severe oral
Speaker 2: ulceration and more critically, any low grade chronic, periopical or
Speaker 2: periodontal infection that a healthy immune system would normally wall
Speaker 2: off into a localized granuloma, It'll just spread exactly, It'll
Speaker 2: suddenly spread through the fascial spaces with terrifying speed. There's
Speaker 2: just no cellular army to contain the bacteria.
Speaker 1: Which brings up a really fascinating contradiction in how we
Speaker 1: manipulate the immune system. Let's talk about systemic cortichosteroids, things
Speaker 1: like dexamethasone or beta methizone. Okay, yeah, we know they're
Speaker 1: potent immunosuppressants, But if they actively shut down the inflammatory cascade,
Speaker 1: wouldn't that technically halt the destructive immune response that causes
Speaker 1: periodontal pocketing Like couldn't it hide gingevitis.
Speaker 2: It's an incredibly deceptive pharmacological paradox. Actually, in the very
Speaker 2: short term, the potent anti inflammatory properties might afford a
Speaker 2: temporary artificial masking of gingal inflammation, so it looks healthy, right.
Speaker 2: The tissue might even look less aerathemitis because of the
Speaker 2: vasodilation and leucoste migration are blocked. But the long term
Speaker 2: physiological cost is devastating to the periodontia.
Speaker 1: Because of the disruption to the bone remodeling cycle.
Speaker 2: Precisely, corticosteroids aggressively tip the scale of bone metabolism. They
Speaker 2: stimulate osteoclastic resorption while simultaneously inducing osteoblastic apoptosis, so they
Speaker 2: literally kill the cells that build new bone. The text
Speaker 2: is definite on this prolonged systemic cordico steroine therapy indece's
Speaker 2: profound drug induced oxteoporosis, which is now classified as a
Speaker 2: major primary risk factor for catastrophic alveolar bone loss. You
Speaker 2: just lose the rigid structural foundation that anchors the.
Speaker 1: Dentician, and because that cell mediated immunity is dialed down,
Speaker 1: those steroids are concurrently masking severe opportunistic infections. Right candidiasis,
Speaker 1: widespread her pedic lesions. Absolutely so, a patient on chronic
Speaker 1: beta methazone who presents with an acute odontogenic infection isn't
Speaker 1: dealing with a routine toothache. It is a time sensitive,
Speaker 1: rapidly spreading threat. The localized inflammatory signs, the heat, the swelling,
Speaker 1: the pain. They might be blunted by the steroids cateratifying. Yeah,
Speaker 1: it lulls the clinician into a false sense of security
Speaker 1: while the infection tracks toward the airway or the cavernous sinus.
Speaker 1: Aggressive local debridement and immediate antibiotic therapy are completely non negotiable.
Speaker 2: Which perfectly illustrates why understanding the systemic baseline is so critical.
Speaker 2: Before we introduce our own pharmacological agents into the mix,
Speaker 2: we have to navigate the dental drug mindfield, starting with
Speaker 2: the most heavily utilized drug in our arsenal.
Speaker 1: Epinephron Epinephrine is the gold standard vasoconstrictor. We rely on
Speaker 1: it to keep the local anesthetic localized to the nerve,
Speaker 1: increase the depth and duration of pulple anesthesia, and provide
Speaker 1: surgical hemostasis, but the systemic absorption is unavoidable. And the
Speaker 1: dictionary outlines a strict three cartridge rule for patients on
Speaker 1: specific cardiovascular medications. Let's look at non selective beta blockers
Speaker 1: drugs like espuctolol or propronolol.
Speaker 2: To understand the interaction here, we have to look at
Speaker 2: the receptor physiology. When we inject exogenous epinephrine, it stimulates
Speaker 2: both alpha one receptors which cause intense vasoconstriction, and beta
Speaker 2: two receptors, which cause vasodilation in the skeletal muscle of vasculature.
Speaker 1: Yeah, so they kind of balance out in a healthy patient.
Speaker 2: Yeah, these opposing actions somewhat balance out the mean arterial pressure.
Speaker 2: But if a patient is taking an on selective beta blocker,
Speaker 2: those beta two receptors are completely blockaded.
Speaker 1: So the epinephrine binds to the alpha one receptors, causing
Speaker 1: massive vasoconstriction, but the compensatory beta two vasodilation is.
Speaker 2: Block exactly, it results in unopposed alpha stimulation. The peripheral
Speaker 2: vascular resistant sky rockets, leading to a sudden, dangerous and
Speaker 2: potentially cerebrovascular event, inducing spike in systolic.
Speaker 1: Blood pressure, which is why the local anesthetic must be
Speaker 1: strictly limited to a maximum of three cartridges injected slowly
Speaker 1: with meticulous aspiration to avoid intravascular delivery, and we see
Speaker 1: that same three cartridge limitation for patients taking non potassium
Speaker 1: sparing diuretics like bendrofluizide or momentinide. These drugs lower blood
Speaker 1: pressure by inhibiting sodium reabsorption in the kidneys, but they
Speaker 1: inevitably drag potassium out with the urine, leaving the patient
Speaker 1: in a state of baseline hypocolemia. How does epinephrine exacerbate that?
Speaker 2: Well, epinefrin actively stimulates the sodium potassium at pase pump
Speaker 2: in skeletal muscle cells. This action forcefully drives extracellular potassium
Speaker 2: into the intracellular space.
Speaker 1: Ah. I see, So, if.
Speaker 2: The patient is already hypoclemic from their diuretic and you
Speaker 2: inject a heavy dose of epinephrine, you drive their serum
Speaker 2: potassium levels down even further, and.
Speaker 1: The heart doesn't like that, not at all.
Speaker 2: Yeah. The myocardial conduction system relies on precise potassium gradients
Speaker 2: to antion. If that gradient collapses, the electrical system misfires,
Speaker 2: exposing the patient to severe, potentially fatal cardiac arrhythmius.
Speaker 1: Okay, let's shift to a class of drugs that carries
Speaker 1: a massive historical stigma in dentistry, monoamine oxidase inhibitors, the
Speaker 1: MAOIs like trannilsipromine used for refractory depression. Aren't we taught
Speaker 1: to be terrified of epinephrine with MAOIs like it would
Speaker 1: trigger an immediate hypertensive crisis.
Speaker 2: Yeah, that is one of the most persistent myths in
Speaker 2: clinical dentistry, and the Dictionary thoroughly debunks it based on
Speaker 2: metabolic pathways.
Speaker 1: Really how so?
Speaker 2: Well, the logic behind the fhere was that MAOIs block
Speaker 2: the breakdown of catacholamines, so adding more catacholamines like epinephrine
Speaker 2: would overload the system. However, exogenous epenipherne, the kind we
Speaker 2: inject from a dental cartridge, is primarily metabolized by a
Speaker 2: completely different enzymatic route. Is broken down by catacol methyl
Speaker 2: transfrase or COMT, which is heavily located in the liver
Speaker 2: and tissues.
Speaker 1: So the monoamine oxidase enzyme isn't even the primary clearance
Speaker 1: mechanism for our local anesthetic.
Speaker 2: Exactly because the COMT pathway remains fully functional. The injected
Speaker 2: epinephrine is cleared efficiently and does not accumulate to toxic levels.
Speaker 2: Standardental local anesthetics with epinephrine are perfectly safe for these patients.
Speaker 1: That's a huge relief it is.
Speaker 2: However, the text explicitly warns that ephedrin, a different sympathy
Speaker 2: almometic sometimes used in emergency management, is a major risk.
Speaker 2: Ephedrin promotes the release of endogenous norbinefhrine from nerve terminals,
Speaker 2: which does rely on monoamine oxidase for breakdown.
Speaker 1: So administering ephedrine to an MAOI patient will cause that
Speaker 1: feared hypertensive crisis. But the lytokane with epinephrine in your
Speaker 1: syringe is metabolically safe. That is a critical distinction between
Speaker 1: exogenous administration and endogenous release.
Speaker 2: Very critical.
Speaker 1: All right, Let's examine the prescriptions we generate chair side
Speaker 1: ns ads and antibiotics. The dictionary lists several absolute contraindications
Speaker 1: for nsides like ibuprofen or neproxin. You cannot prescribe them
Speaker 1: to patients taking allandronic acid, systemic cortichosteroids, or sucral fate.
Speaker 2: Yeah, all three of those systemic medications inherently compromise the
Speaker 2: integrity of the gastrointestinal mucosa. NSAIDs function by inhibiting the
Speaker 2: cyclogenes enzymes, particularly kox one, which is responsible for synthesizing
Speaker 2: the protective prostic landins that maintain the stomach's mucosal barrier.
Speaker 1: So you combine them and its disaster.
Speaker 2: Right. When you combine an NSAID with abysphosphinit or a steroid,
Speaker 2: you completely strip away the gastric defenses, creating a synergistic
Speaker 2: catastrophic risk for severe peptic ulceration and massive gastrointestinal hemorrhage.
Speaker 1: When the prostaglandin inhibition isn't just a gastintestinal issue either,
Speaker 1: it heavily impacts renal hemodynamics. Nsais actively antagonize the hypotensive
Speaker 1: effects of blood pressure medications like methyl dopa and przosin.
Speaker 2: Yeah, the kidneys rely on those same prostaglandins to maintain
Speaker 2: renal blood flow and facilitate sodium excretion. By inhibiting prostaglandin synthesis,
Speaker 2: n sides cause renal vasoconstriction and sodium retention, directly counteracting
Speaker 2: the pharmacological mechanisms of the anti hypertensis.
Speaker 1: So you can significantly elevate a patient's blood pressure over
Speaker 1: the course of a few days, just by prescribing ibuprofen
Speaker 1: for post operative pains easily. What about the antibiotic cascades.
Speaker 1: We know tetracyclines are notoriously unstable in the gastriin testinal tract.
Speaker 2: They are highly susceptible to chellation. If a patient is
Speaker 2: taking aluminium hydroxide as a daily antacid, or a polysaccharide
Speaker 2: iron complex for anemia, the presence of those polyvalent medications
Speaker 2: in the gut is highly problematic.
Speaker 1: They bind together exactly.
Speaker 2: The tetracyclin molecules bind tightly to the aluminum or iron ions,
Speaker 2: forming massive insoluble complexes that just cannot cross the intestinal mucosa.
Speaker 2: The antibiotic absorption is completely integated, It passes through the
Speaker 2: GI tract unabsorbed, and your odontogenic infection continues to spread unhindered.
Speaker 1: Wow, And you know, if we're doing sedation, we have
Speaker 1: to look at metazolam and diazepam too. They rely heavily
Speaker 1: on hepatic clearance. The dictionary highlights severe interactions with drugs
Speaker 1: like verapamil, a calcium channel blocker, and rotonovir an HIV
Speaker 1: protase inhibitor. Now, a dentist might look at rotonovir, an
Speaker 1: antiviral drug, and assume it has absolutely zero overlap with
Speaker 1: the benzodiazepine sedative.
Speaker 2: You'd think so, but it comes down to the cytochrome
Speaker 2: P four fifty enzyme system in the liver. Specifically, the
Speaker 2: CYP three A four isoenzyme. Mitazoone is heavily dependent on
Speaker 2: CYP three A four for its metabolism and clearance from
Speaker 2: the bloodstream, and.
Speaker 1: Let me guess those drugs inhibit it.
Speaker 2: Both verapamil and rotonivir are potent inhibitors of that specific enzyme.
Speaker 2: If you administer a standard weight based dose of midazolam
Speaker 2: to a patient on retonivir, the livers simply cannot process it.
Speaker 1: So the sedative effects doesn't just last longer, it compounds.
Speaker 2: The plasma concentration of midazolam skyrockets, leading to prolonged, profound
Speaker 2: sedation and a massive risk of severe respiratory depression. You
Speaker 2: are navigating blind if you don't account for a paddic
Speaker 2: enzyme inhibition.
Speaker 1: So what's the protocol there?
Speaker 2: The clinical protocol mandates drastically lowered doses of the sedative
Speaker 2: titrated incredibly slowly with continuous pulse oxymmetry and cabnography monitoring.
Speaker 1: That brings us perfectly to the logistical reality of treating
Speaker 1: these patients. How do these complex pharmacological profiles dictate the
Speaker 1: physical chair side management? Let's analyze the diabetic patient. We're
Speaker 1: looking at oral antidiabetics, sulfonylurias like libin chlamide, or big
Speaker 1: one eyes like met Foreman. The primary acute threat during
Speaker 1: a dental appointment is a hypoglycemic crisis right ll Yes.
Speaker 2: Dental anxiety often completely disrupts a patient's routine. They skip
Speaker 2: breakfast because they're nervous or because they mistakenly believe they
Speaker 2: need an empty stomach for a local anisset of procedure,
Speaker 2: but they still take their glibin comide, Their endogenous insulin spikes,
Speaker 2: the LOGOS drops, and they crash in the chair. The
Speaker 2: logistical management requires scheduling these patients in the early to
Speaker 2: mid morning, during the most stable phase of their glycemic cycle,
Speaker 2: verifying chlored intake before ever reclining the chair, and having
Speaker 2: oral glucose gells immediately accessible.
Speaker 1: But the dictionary points out something wild. Our own prescriptions
Speaker 1: can actively manipulate their glycemic control. High dose aspirin and
Speaker 1: certain enosides can actually induce hypoglycemia in patients taking sulfonuluria.
Speaker 2: Yeah nisides are highly protein bound in the plasma. They
Speaker 2: can physically displace the sulfonilaria molecules from the plasma proteins.
Speaker 1: So it makes the diabetic drug stronger.
Speaker 2: This sudden increase in the unbound active fraction of the
Speaker 2: diabetic drug artificially amplifies its effect, driving the blood glucose
Speaker 2: down danger low WOW. Conversely, if you prescribe a short
Speaker 2: course of corticosteroids to manage severe post operative edema, steroids
Speaker 2: stimulate gluconeogenesis and induce peripheral insulin resistance. They aggressively antagonize
Speaker 2: the diabetic medication, causing a sharp spike in hyperglycemia. You
Speaker 2: cannot prescribe blindly in the population.
Speaker 1: Let's apply that same logistical scrutiny to the respiratory patient
Speaker 1: someone presenting with severe asthma or COPD managed with broncho
Speaker 1: dilators like aminofolline or sealbutamol. From a purely mechanical standpoint,
Speaker 1: positioning is critical.
Speaker 2: Very you must avoid placing these patients in a fully
Speaker 2: supline position. When they are laid flat, the adominal viscera
Speaker 2: compress against the.
Speaker 1: Diaphragm, which makes breathing harder.
Speaker 2: For a patient whose forced expiratory volume is already severely
Speaker 2: compromised by broncho constriction or alveolar degradation, that mechanical pressure
Speaker 2: against the diaphragm can rapidly induce respiratory distress. You have
Speaker 2: to maintain them in a semi supine or upright position
Speaker 2: to allow maximum diaphramatic excursion.
Speaker 1: The dictionary also highlights two significant chemical triggers for asthmatics
Speaker 1: that we utilize constantly. First, a well documented cross reactivity
Speaker 1: or a significant percentage of asthmatic patients possess an intrinsic
Speaker 1: allergy to aspirin, which can precipitate an immediate severe bronchospasm. Second,
Speaker 1: the hidden trap in our local anesthetic cartridges sulfite preservatives.
Speaker 2: This is a huge one. Epinephrine is highly unstable and
Speaker 2: oxidizes rapidly. To prevent this, manufacturers add sodium metabosulfite to
Speaker 2: any local anesthetic cartridge containing a vasoconstrictor O. A subset
Speaker 2: of asthmatic patients are severely allergic to these sulfide preservatives,
Speaker 2: So the very injection you are using to achieve profound
Speaker 2: anesthesia could instantly trigger a severe asthmatic crisis.
Speaker 1: So what's the workaround?
Speaker 2: If they have a known sulfite allergy? You are restricted
Speaker 2: to using plain local anesthetics without epinephrine like three percent mapivacane,
Speaker 2: which dramatically reduces your working time and eliminates surgical heat.
Speaker 1: Mosttases and additionally, the physical tools we use can compromise
Speaker 1: their airway. Placing a rubber dam is the standard of
Speaker 1: care for ENDO and restorative isolation, but it completely includes
Speaker 1: the oral airway. For a severe asthmatic or a COPD
Speaker 1: patient who relies on accessory oral breathing, a rubber dam
Speaker 1: can severely embarrass their respiration. If isolation is non negotiable
Speaker 1: for the procedure, the protocol mandates providing supplemental oxygen via
Speaker 1: a nasal canula throughout the entire appointment to maintain their
Speaker 1: oxygen saturation.
Speaker 2: And Logistical management is also about infection control, particularly with tuberculosis.
Speaker 2: If a patient's medical history reveals active TB, management with
Speaker 2: drugs like if ambatol isoni acid or rafambitsin the protocol
Speaker 2: is absolute. Elective dental care is strictly contraindicated.
Speaker 1: You postpone everything until they are medically cleared. But they
Speaker 1: present with an acute dental emergency like a severe facial
Speaker 1: swelling or intractable pain, you're obligated to tree.
Speaker 2: In that emergency scenario. You have to manage the aerosolization risk.
Speaker 2: The high speed hand piece and ultrasonic scaler create a
Speaker 2: massive aerosol cloud that can easily disseminate the mycobacteria throughout
Speaker 2: the operatory. Right, you must utilize a rubber dam to
Speaker 2: isolate the operating field from the pulmonary tract, assuming their
Speaker 2: airway can tolerate it and operate under high volume evacuation
Speaker 2: with full N ninety five particulate respirators and fee shields.
Speaker 1: We've mapped out a massive amount of pharmacological data today
Speaker 1: from receptor pathways to hepatic enzyme inhibition. So to solidify
Speaker 1: these concepts for you listening, let's run a quick clinical
Speaker 1: review exercise. Say you are treating a patient who requires
Speaker 1: a surgical abstraction of a mendimular molar. Their medical history
Speaker 1: indicates they are currently taking a subutalol, a non selective
Speaker 1: beta blocker, and benjo fluizide, a thighzid diuretic. Based on
Speaker 1: the Drug Dictionary for dentistry, what are your specific limitations
Speaker 1: regarding local anesthesia and what highly common class of post
Speaker 1: operative analgesics must use absolutely avoid prescribing.
Speaker 2: Well, let's synthesize the pathways we've discussed. For the local anesthesia,
Speaker 2: the presence of the non selected beta blocker and the
Speaker 2: non potassium spearing diuretic triggers the rigid three cartridge maximum
Speaker 2: rule for epinephrin.
Speaker 1: Because of the blood pressure spike right.
Speaker 2: Exactly Exceeding this limit forces the exogenous epinephrine to bind
Speaker 2: to the alpha one receptors while the beta two receptors
Speaker 2: are blocked, risking a catastrophic spike in peripheral vascular resistance
Speaker 2: and systolic blood pressure. Simultaneously, the ebenephrine will aggressively drive
Speaker 2: extracelluar potassium into the cells, compounding the diuretic, induce hypokalemia
Speaker 2: and exposing the patient to severe cardiac arrhythmius.
Speaker 1: And for the post operative pain management, you must completely
Speaker 1: avoid prescribing any nsades, including abuprofen or naoproxin.
Speaker 2: The NSAS will inhibit the renal prostag landins required for
Speaker 2: renal blood flow, directly antagonizing the hypotensive effects of both
Speaker 2: the beta blocker and the diuretic. Furthermore, combining an NSAID
Speaker 2: with a THIAZI diuretic heavily compounds the risk of acute nephrotoxicity.
Speaker 2: You would need to rely on paracetamol potentially combined with
Speaker 2: the centrally acting analgetic, carefully weighing the patient's hepatic and
Speaker 2: respiratory status.
Speaker 1: That is the essence of applied clinical pharmacology. You aren't
Speaker 1: just reciting side effects. You know, you're actively engineering a
Speaker 1: safe biological pathway through a compromised systemic environment.
Speaker 2: Because knowledge in this field is only valuable when it
Speaker 2: dictates action. And the final clinical reality we have to
Speaker 2: acknowledge is that this environment is evolving faster than ever before.
Speaker 2: We are already seeing the leading edge of biologics entering
Speaker 2: the dictionary monoclonal antibodies like palavizoomap as.
Speaker 1: The medical field transitions away from traditional small molecule drugs
Speaker 1: and accelerates into highly complex, genetically targeted immunotherapies, and biologics.
Speaker 1: The dental landscape is going to shift radically. The systemic
Speaker 1: baseline of your patients is going to become exponentially more complex.
Speaker 2: We are rapidly approaching an era where referencing a printed
Speaker 2: dictionary while enough. The future of clinical dentistry will likely
Speaker 2: require running real time chair side pharmacogenomic profiles.
Speaker 1: Like seeing how their genes will react.
Speaker 2: Exactly analyzing how a patient's specific genetic expression will metabolize
Speaker 2: and react to our interventions before we can safely administer
Speaker 2: a single drop of lytokine. The intersection of systemic medicine
Speaker 2: and dental surgery is only going to deepen.
Speaker 1: Because in the modern clinic, what fixes the bone might
Speaker 1: just break the system. Something for you to think about
Speaker 1: until next time. Keep digging deeper