WEBVTT 1 00:00:00.120 --> 00:00:02.399 You know, usually when we look at a dental diagnosis, 2 00:00:02.439 --> 00:00:06.719 there's this expectation of clinical precision. 3 00:00:06.400 --> 00:00:07.919 Right like an engineering mindset. 4 00:00:08.080 --> 00:00:10.720 Exactly like a patient comes in with a fractured cusp, 5 00:00:11.160 --> 00:00:14.160 the radiograph shows that jagged white line and you point 6 00:00:14.160 --> 00:00:15.800 to it on the monitor and say, well, there it is. 7 00:00:16.079 --> 00:00:20.239 That's the structural failure. It's clean, it's isolated, and honestly 8 00:00:20.280 --> 00:00:21.000 it's comforting. 9 00:00:21.160 --> 00:00:23.800 It creates an illusion of control. Really. I mean, we're 10 00:00:23.839 --> 00:00:27.120 trained to operate in millimeters, focusing so intensely on the 11 00:00:27.120 --> 00:00:32.200 hard tissues in the immediate periodontium. But the reality of 12 00:00:32.240 --> 00:00:34.840 otter and clinical practice is just far less isolated. 13 00:00:34.960 --> 00:00:36.880 Yeah, because then you look down at the patient's medical 14 00:00:36.960 --> 00:00:40.719 history form and that neat structural mindset just completely shatters. 15 00:00:40.880 --> 00:00:41.479 It really does. 16 00:00:41.679 --> 00:00:45.000 Suddenly you aren't just treating a fractured tooth or you know, 17 00:00:45.119 --> 00:00:49.880 a coufurious lesion. You're operating inside this highly complex systemic 18 00:00:50.000 --> 00:00:54.039 environment that has been fundamentally re engineered by prescription drugs. 19 00:00:54.600 --> 00:00:56.759 And for you listening to this deep dive as a 20 00:00:56.840 --> 00:01:01.240 dental student or young professional, navigating that pharmacological landscape is 21 00:01:01.399 --> 00:01:05.000 quite literally the difference between a routine procedure and a 22 00:01:05.040 --> 00:01:06.719 life threatening medical emergency. 23 00:01:07.000 --> 00:01:10.599 Absolutely, And that's exactly why the Drug Dictionary for Dentistry 24 00:01:10.599 --> 00:01:14.159 by Mitchen and Seymour is so vital. It establishes a 25 00:01:14.159 --> 00:01:16.719 core philosophy for this exact reality. Right. 26 00:01:16.760 --> 00:01:19.280 Our mission today is to pull the real world clinical 27 00:01:19.319 --> 00:01:22.239 pearls from this guide, right, not just read a list. 28 00:01:22.439 --> 00:01:25.959 Yeah, we have to move beyond just memorizing alphabetical lists 29 00:01:25.959 --> 00:01:28.680 of side effects. I mean, a patient's medical history isn't 30 00:01:28.680 --> 00:01:32.000 just a background check. It's the ultimate, non negotiable blueprint 31 00:01:32.000 --> 00:01:34.760 for their dental treatment plan. We need to understand the 32 00:01:34.879 --> 00:01:38.719 underlying physiological mechanisms, like the why and the how, because 33 00:01:38.719 --> 00:01:40.680 that is what dictates clinical management. 34 00:01:40.840 --> 00:01:42.920 So we're going to break this down into four clinical 35 00:01:42.959 --> 00:01:46.719 pillars today. Let's start with the immediate oral environment. When 36 00:01:46.760 --> 00:01:48.920 a patient opens their mouth, before you even pick up 37 00:01:48.959 --> 00:01:53.079 an explorer, you're often looking at a chemically altered landscape. Oh, 38 00:01:53.480 --> 00:01:57.239 like we see zerostomia constantly. But we need to look 39 00:01:57.280 --> 00:02:01.680 past the obvious discomfort. You know, saliva isn't just lubrication. 40 00:02:02.280 --> 00:02:05.200 I always compare a mouth without saliva to a car 41 00:02:05.200 --> 00:02:09.759 engine running without oil. You get friction, decay, and eventual breakdown. 42 00:02:10.080 --> 00:02:13.439 It's a continuous buffering liquid immune system. 43 00:02:13.639 --> 00:02:16.120 That's a great analogy. Yeah, and when that salivary flow 44 00:02:16.159 --> 00:02:19.800 is suppressed, you are stripping away the primary defense mechanism 45 00:02:20.120 --> 00:02:25.919 against demineralization and opportunistic pathogens. The text emphasizes how ubiquitous 46 00:02:25.960 --> 00:02:31.599 this parasympathetic inhibition is across vastly different pharmacological classes. I mean, 47 00:02:31.599 --> 00:02:35.000 you see severe salivary flow reduction with tricyclic antidepressants like 48 00:02:35.000 --> 00:02:38.000 amatrypti line in disulibin, which are so calmon very common, 49 00:02:38.520 --> 00:02:43.520 and antipsychotics like amazyl pride and quishiapine, and histamines like acrovastine, 50 00:02:43.719 --> 00:02:48.360 even asima medications like amtophyline. They all disrupt the autonomic 51 00:02:48.479 --> 00:02:50.759 pathways that stimulate the salivary glands. 52 00:02:50.960 --> 00:02:53.879 So the buffering capacity plummets, the oral pH drocks and 53 00:02:53.919 --> 00:02:57.520 you get this massive carryogenic shift. Clinically, if that patient 54 00:02:57.599 --> 00:03:00.479 is dentate, you can't just suggest they rank a little 55 00:03:00.479 --> 00:03:00.879 more water. 56 00:03:01.000 --> 00:03:01.759 No, definitely not. 57 00:03:02.039 --> 00:03:06.000 They require an immediate, aggressive, high carries risk protocol, so 58 00:03:06.439 --> 00:03:14.039 prescription topical fluorides, remineralizing pastes, artificial saliva, and for addentialist patients, 59 00:03:14.080 --> 00:03:16.639 the prosodonic implications are just disastrous. 60 00:03:16.759 --> 00:03:17.960 Oh, it ruins the retention. 61 00:03:18.400 --> 00:03:21.759 Yeah, you lose that crucial microscopic layer of saliva, which 62 00:03:21.800 --> 00:03:24.759 means you lose the surface tension and capillary action required 63 00:03:24.759 --> 00:03:28.439 for denture attention. The acrylic just won't seal to the mucosa. 64 00:03:28.639 --> 00:03:32.639 It destabilizes the entire restorative foundation. And while salvary suppression 65 00:03:32.639 --> 00:03:36.840 alters the biochemical environment, other systemic drugs are aggressively altering 66 00:03:36.879 --> 00:03:39.639 the physical architecture of the hard and soft tissues. 67 00:03:39.400 --> 00:03:40.680 Like gingibal overgrowth. 68 00:03:40.840 --> 00:03:45.360 Exactly. We learn early on about fennytoin and gingibal overgrowth, 69 00:03:45.560 --> 00:03:49.719 which is driven by an alteration in fibroblast metabolism, but 70 00:03:49.800 --> 00:03:53.400 the dictionary highlights far more insidious structural defects caused by 71 00:03:53.400 --> 00:03:54.520 this anti convulsant. 72 00:03:54.639 --> 00:03:57.159 Wait, like what the root architecture changes? 73 00:03:57.240 --> 00:04:00.759 Right? It does. Yeah, finnytoin is associated with severe root shortening, 74 00:04:01.000 --> 00:04:05.439 root resorption, and hyper semintosis. You get this massive excessive 75 00:04:05.439 --> 00:04:08.879 deposition of cementum along the apical third of the roots. 76 00:04:09.280 --> 00:04:12.960 Wow, Okay, so clinically that's a nightmare for extractions. 77 00:04:12.599 --> 00:04:14.680 Right, if you're planning an extraction on a patient with 78 00:04:14.719 --> 00:04:18.279 a long history of fennytoyin use. What looks like a straightforward, 79 00:04:18.319 --> 00:04:21.360 simple elevation on the radiograph will often turn into a 80 00:04:21.399 --> 00:04:26.759 brutal surgical extraction because that hyper seminosis essentially anchors the 81 00:04:26.800 --> 00:04:29.279 tooth into the alveolar bone like a rivet. 82 00:04:29.399 --> 00:04:30.720 That's crazy to think about. 83 00:04:31.199 --> 00:04:34.879 And additionally, for female patients of child bearing age, finny 84 00:04:34.879 --> 00:04:38.199 toyin carries a heavily documented to ratogenic risk for cleft, 85 00:04:38.240 --> 00:04:39.000 lip and palate. 86 00:04:39.199 --> 00:04:42.199 Right, and we also see significant tissue alterations with calcium 87 00:04:42.279 --> 00:04:43.519 channel blockers too, don't we. 88 00:04:43.639 --> 00:04:46.759 Yeah, Drugs like is ratifine and then sold to pain they. 89 00:04:46.639 --> 00:04:51.360 Interfere with intracellular calcium mobilization, which somehow triggers that same 90 00:04:51.519 --> 00:04:57.879 pronounced anterior gingibal overgrowth, completely complicating oral hygiene and periodonal maintenance. 91 00:04:57.920 --> 00:04:59.639 It's a very visible side effect. 92 00:04:59.319 --> 00:05:02.040 But let's look at it much more acute volatile tissue 93 00:05:02.040 --> 00:05:06.600 reaction angioedema the sudden massive swelling of the lips, tongue, 94 00:05:06.600 --> 00:05:09.800 and the floor of the mouth. The text flags ace 95 00:05:10.160 --> 00:05:15.839 inhibitors like solazeprol and bisphosphonse like allandronic acid as primary triggers. 96 00:05:15.920 --> 00:05:17.199 Yes, this is a critical one. 97 00:05:17.279 --> 00:05:20.040 Now in a high stress scenario. If a patient's tongue 98 00:05:20.040 --> 00:05:23.920 starts swelling rapidly in the chair, instinct dictates grabbing the 99 00:05:23.959 --> 00:05:26.639 emergency kit, hitting them with an EpiPen, and falling up 100 00:05:26.680 --> 00:05:30.040 with hedrochurtisome. But the literature suggests that's a trap. Right. 101 00:05:30.240 --> 00:05:32.800 Why does standard anaphylaxis protocol fail here? 102 00:05:33.040 --> 00:05:36.160 Because the mechanism of action is fundamentally different from a 103 00:05:36.199 --> 00:05:39.680 type bi hypersensitivity reaction. Oh so, if a patient is 104 00:05:39.720 --> 00:05:43.680 allergic to penicillin, you have an IgE mediated response causing 105 00:05:43.800 --> 00:05:47.639 mass cells to degranulate and release massive amounts of histamine. 106 00:05:47.680 --> 00:05:49.160 Right, and that's where the epinephrin comes in. 107 00:05:49.519 --> 00:05:55.680 Exactly. Epinephrine and corticosteroids aggressively target and reverse that histamine pathway. 108 00:05:55.839 --> 00:06:02.240 But ace inhibitor induced angioedema is not mediator by histamin Oh. Interesting, Yeah, 109 00:06:02.319 --> 00:06:06.199 ace engie intents and converting enzyme is also responsible for 110 00:06:06.240 --> 00:06:11.279 breaking down bradikeinan, which is a potent endogenous phasodilator. When 111 00:06:11.279 --> 00:06:15.519 you inhibit ace, brite akeenin accumulates in the tissues, leading 112 00:06:15.560 --> 00:06:17.839 to massive fluid extravasation and swelling. 113 00:06:18.519 --> 00:06:21.600 So hitting them with epinephrine does absolutely nothing for the 114 00:06:21.600 --> 00:06:22.639 brandikeine accumulation. 115 00:06:22.920 --> 00:06:26.399 It is functionally useless in this specific pathway, the swelling 116 00:06:26.439 --> 00:06:29.759 will just continue despite the adrenaline. Wow. This is why 117 00:06:29.759 --> 00:06:33.199 you must proactively question patients on ace inhibitors about any 118 00:06:33.279 --> 00:06:37.639 history of transient swelling, swallowing difficulties, or airway embarrassment before 119 00:06:37.680 --> 00:06:42.319 initiating treatment. Even minor dental trauma or local anesthetic injections 120 00:06:42.480 --> 00:06:44.959 can precipitate this bratikin and mediated crisis. 121 00:06:45.000 --> 00:06:48.639 Okay, so we've got mucosal swelling, structural changes, and salivary collapse. 122 00:06:48.680 --> 00:06:50.680 But let's pivot. That's just the surface level, right, that's 123 00:06:50.720 --> 00:06:52.959 what we can see. Yeah, if you're planning any sort 124 00:06:53.000 --> 00:06:57.120 of invasive procedure and extraction, implant placement, or pyioflap surgery, 125 00:06:57.920 --> 00:07:01.079 the real threat is what's happening beneath the mucosa in 126 00:07:01.120 --> 00:07:02.160 the blood and bone. 127 00:07:02.240 --> 00:07:06.639 The hemenotological environment literally dictates your surgical success or failure. 128 00:07:07.519 --> 00:07:11.800 The dictionary establishes a rigid clinical threshold here, it's the 129 00:07:12.199 --> 00:07:14.120 less than one hundred thousand platelet rule. 130 00:07:14.079 --> 00:07:17.040 Right, Because we're looking at a massive spectrum of drugs 131 00:07:17.079 --> 00:07:21.639 that induce bone marrow suppression. Chemotherapeutic agents like eclarubasin and 132 00:07:21.680 --> 00:07:25.360 carboplatin are expected obviously sure, but the list extends to 133 00:07:25.560 --> 00:07:30.480 rheumatology drugs like penicillamine and psychiatric medications like maprobamate. They 134 00:07:30.480 --> 00:07:35.040 trigger profound frombocyopenia, a granular of cytosis and lekopenia. 135 00:07:35.120 --> 00:07:37.959 And you know, the physiology of hemostasis relies heavily on 136 00:07:38.000 --> 00:07:41.120 that initial platelet plug to form the scaffold for the 137 00:07:41.120 --> 00:07:45.000 coagulation cascade. Once a patient's platelet count drops below one 138 00:07:45.040 --> 00:07:49.120 hundred thousand per micro leader, normal physiological clotting mechanisms become 139 00:07:49.160 --> 00:07:50.279 fundamentally inadequate. 140 00:07:50.279 --> 00:07:52.920 For dental surgery, a routine extraction site will simply not 141 00:07:52.959 --> 00:07:54.519 stop oozing exactly. 142 00:07:54.639 --> 00:07:57.480 You have to step in and artificially manufacture hemostasis. You 143 00:07:57.519 --> 00:07:59.759 can't just place a cotton roll and rely on pressure. 144 00:08:00.120 --> 00:08:00.800 So what do you do? 145 00:08:01.000 --> 00:08:05.160 You need to actively pack the socket with oxidized, regenerated 146 00:08:05.160 --> 00:08:09.839 cellulose or gelatin sponges, place Figure eight tension sutures to 147 00:08:09.920 --> 00:08:13.720 physically approximate the tissue, and have the logistical groundwork laid 148 00:08:13.800 --> 00:08:18.759 to request an immediate plately transfusion if refractory bleeding occurs. 149 00:08:18.560 --> 00:08:21.600 Right, and that bone marrow suppression isn't just about platelets. 150 00:08:21.639 --> 00:08:23.639 We also mention a granular cytosis. 151 00:08:23.759 --> 00:08:27.240 Yeah, stripping away the granular lecocytes, the NEUTROPHILSI, asenophils, and 152 00:08:27.279 --> 00:08:31.120 basophyls means the patient has lost their cellular first responders. 153 00:08:31.879 --> 00:08:33.559 So clinically, what does that look like? 154 00:08:33.720 --> 00:08:38.320 Clinically? This manifests as a staggering susceptibility to severe oral 155 00:08:38.399 --> 00:08:43.360 ulceration and more critically, any low grade chronic, periopical or 156 00:08:43.399 --> 00:08:47.039 periodontal infection that a healthy immune system would normally wall 157 00:08:47.039 --> 00:08:50.399 off into a localized granuloma, It'll just spread exactly, It'll 158 00:08:50.399 --> 00:08:53.759 suddenly spread through the fascial spaces with terrifying speed. There's 159 00:08:53.840 --> 00:08:56.799 just no cellular army to contain the bacteria. 160 00:08:56.360 --> 00:08:59.360 Which brings up a really fascinating contradiction in how we 161 00:08:59.480 --> 00:09:04.679 manipulate the immune system. Let's talk about systemic cortichosteroids, things 162 00:09:04.720 --> 00:09:08.320 like dexamethasone or beta methizone. Okay, yeah, we know they're 163 00:09:08.399 --> 00:09:13.120 potent immunosuppressants, But if they actively shut down the inflammatory cascade, 164 00:09:13.240 --> 00:09:17.960 wouldn't that technically halt the destructive immune response that causes 165 00:09:18.159 --> 00:09:21.279 periodontal pocketing Like couldn't it hide gingevitis. 166 00:09:21.559 --> 00:09:26.080 It's an incredibly deceptive pharmacological paradox. Actually, in the very 167 00:09:26.080 --> 00:09:29.200 short term, the potent anti inflammatory properties might afford a 168 00:09:29.240 --> 00:09:33.799 temporary artificial masking of gingal inflammation, so it looks healthy, right. 169 00:09:33.879 --> 00:09:36.279 The tissue might even look less aerathemitis because of the 170 00:09:36.360 --> 00:09:40.399 vasodilation and leucoste migration are blocked. But the long term 171 00:09:40.440 --> 00:09:43.919 physiological cost is devastating to the periodontia. 172 00:09:43.480 --> 00:09:46.320 Because of the disruption to the bone remodeling cycle. 173 00:09:46.440 --> 00:09:51.159 Precisely, corticosteroids aggressively tip the scale of bone metabolism. They 174 00:09:51.200 --> 00:09:57.080 stimulate osteoclastic resorption while simultaneously inducing osteoblastic apoptosis, so they 175 00:09:57.120 --> 00:09:59.519 literally kill the cells that build new bone. The text 176 00:09:59.519 --> 00:10:05.120 is definite on this prolonged systemic cordico steroine therapy indece's 177 00:10:05.159 --> 00:10:09.840 profound drug induced oxteoporosis, which is now classified as a 178 00:10:09.960 --> 00:10:14.720 major primary risk factor for catastrophic alveolar bone loss. You 179 00:10:14.840 --> 00:10:17.639 just lose the rigid structural foundation that anchors the. 180 00:10:17.679 --> 00:10:21.360 Dentician, and because that cell mediated immunity is dialed down, 181 00:10:21.679 --> 00:10:27.080 those steroids are concurrently masking severe opportunistic infections. Right candidiasis, 182 00:10:27.399 --> 00:10:31.159 widespread her pedic lesions. Absolutely so, a patient on chronic 183 00:10:31.240 --> 00:10:35.600 beta methazone who presents with an acute odontogenic infection isn't 184 00:10:35.639 --> 00:10:38.279 dealing with a routine toothache. It is a time sensitive, 185 00:10:38.480 --> 00:10:42.879 rapidly spreading threat. The localized inflammatory signs, the heat, the swelling, 186 00:10:42.919 --> 00:10:46.000 the pain. They might be blunted by the steroids cateratifying. Yeah, 187 00:10:46.039 --> 00:10:48.399 it lulls the clinician into a false sense of security 188 00:10:48.399 --> 00:10:51.440 while the infection tracks toward the airway or the cavernous sinus. 189 00:10:52.000 --> 00:10:56.960 Aggressive local debridement and immediate antibiotic therapy are completely non negotiable. 190 00:10:56.519 --> 00:11:00.480 Which perfectly illustrates why understanding the systemic baseline is so critical. 191 00:11:00.799 --> 00:11:03.720 Before we introduce our own pharmacological agents into the mix, 192 00:11:04.039 --> 00:11:07.039 we have to navigate the dental drug mindfield, starting with 193 00:11:07.080 --> 00:11:09.559 the most heavily utilized drug in our arsenal. 194 00:11:09.320 --> 00:11:13.600 Epinephron Epinephrine is the gold standard vasoconstrictor. We rely on 195 00:11:13.639 --> 00:11:16.120 it to keep the local anesthetic localized to the nerve, 196 00:11:16.279 --> 00:11:19.639 increase the depth and duration of pulple anesthesia, and provide 197 00:11:19.679 --> 00:11:24.279 surgical hemostasis, but the systemic absorption is unavoidable. And the 198 00:11:24.320 --> 00:11:27.879 dictionary outlines a strict three cartridge rule for patients on 199 00:11:28.000 --> 00:11:33.080 specific cardiovascular medications. Let's look at non selective beta blockers 200 00:11:33.159 --> 00:11:35.919 drugs like espuctolol or propronolol. 201 00:11:36.080 --> 00:11:38.000 To understand the interaction here, we have to look at 202 00:11:38.000 --> 00:11:43.159 the receptor physiology. When we inject exogenous epinephrine, it stimulates 203 00:11:43.159 --> 00:11:47.360 both alpha one receptors which cause intense vasoconstriction, and beta 204 00:11:47.399 --> 00:11:51.720 two receptors, which cause vasodilation in the skeletal muscle of vasculature. 205 00:11:51.879 --> 00:11:54.320 Yeah, so they kind of balance out in a healthy patient. 206 00:11:54.600 --> 00:11:58.360 Yeah, these opposing actions somewhat balance out the mean arterial pressure. 207 00:11:58.600 --> 00:12:01.360 But if a patient is taking an on selective beta blocker, 208 00:12:01.519 --> 00:12:03.799 those beta two receptors are completely blockaded. 209 00:12:04.039 --> 00:12:07.679 So the epinephrine binds to the alpha one receptors, causing 210 00:12:07.799 --> 00:12:12.399 massive vasoconstriction, but the compensatory beta two vasodilation is. 211 00:12:12.559 --> 00:12:17.320 Block exactly, it results in unopposed alpha stimulation. The peripheral 212 00:12:17.399 --> 00:12:21.559 vascular resistant sky rockets, leading to a sudden, dangerous and 213 00:12:21.600 --> 00:12:25.360 potentially cerebrovascular event, inducing spike in systolic. 214 00:12:24.879 --> 00:12:27.759 Blood pressure, which is why the local anesthetic must be 215 00:12:27.759 --> 00:12:31.720 strictly limited to a maximum of three cartridges injected slowly 216 00:12:31.960 --> 00:12:36.080 with meticulous aspiration to avoid intravascular delivery, and we see 217 00:12:36.120 --> 00:12:39.759 that same three cartridge limitation for patients taking non potassium 218 00:12:39.759 --> 00:12:44.679 sparing diuretics like bendrofluizide or momentinide. These drugs lower blood 219 00:12:44.679 --> 00:12:47.960 pressure by inhibiting sodium reabsorption in the kidneys, but they 220 00:12:48.000 --> 00:12:51.120 inevitably drag potassium out with the urine, leaving the patient 221 00:12:51.159 --> 00:12:55.480 in a state of baseline hypocolemia. How does epinephrine exacerbate that? 222 00:12:55.679 --> 00:12:59.759 Well, epinefrin actively stimulates the sodium potassium at pase pump 223 00:13:00.080 --> 00:13:04.919 in skeletal muscle cells. This action forcefully drives extracellular potassium 224 00:13:05.200 --> 00:13:06.720 into the intracellular space. 225 00:13:06.919 --> 00:13:08.200 Ah. I see, So, if. 226 00:13:08.080 --> 00:13:11.159 The patient is already hypoclemic from their diuretic and you 227 00:13:11.240 --> 00:13:13.960 inject a heavy dose of epinephrine, you drive their serum 228 00:13:14.000 --> 00:13:15.919 potassium levels down even further, and. 229 00:13:15.879 --> 00:13:17.759 The heart doesn't like that, not at all. 230 00:13:17.879 --> 00:13:21.919 Yeah. The myocardial conduction system relies on precise potassium gradients 231 00:13:22.039 --> 00:13:25.960 to antion. If that gradient collapses, the electrical system misfires, 232 00:13:26.039 --> 00:13:30.399 exposing the patient to severe, potentially fatal cardiac arrhythmius. 233 00:13:30.440 --> 00:13:33.000 Okay, let's shift to a class of drugs that carries 234 00:13:33.039 --> 00:13:38.720 a massive historical stigma in dentistry, monoamine oxidase inhibitors, the 235 00:13:38.840 --> 00:13:43.519 MAOIs like trannilsipromine used for refractory depression. Aren't we taught 236 00:13:43.559 --> 00:13:46.360 to be terrified of epinephrine with MAOIs like it would 237 00:13:46.399 --> 00:13:48.480 trigger an immediate hypertensive crisis. 238 00:13:48.559 --> 00:13:50.679 Yeah, that is one of the most persistent myths in 239 00:13:50.759 --> 00:13:53.840 clinical dentistry, and the Dictionary thoroughly debunks it based on 240 00:13:53.919 --> 00:13:54.919 metabolic pathways. 241 00:13:55.000 --> 00:13:55.759 Really how so? 242 00:13:56.080 --> 00:13:59.440 Well, the logic behind the fhere was that MAOIs block 243 00:13:59.519 --> 00:14:04.080 the breakdown of catacholamines, so adding more catacholamines like epinephrine 244 00:14:04.240 --> 00:14:08.919 would overload the system. However, exogenous epenipherne, the kind we 245 00:14:08.960 --> 00:14:12.759 inject from a dental cartridge, is primarily metabolized by a 246 00:14:12.799 --> 00:14:16.519 completely different enzymatic route. Is broken down by catacol methyl 247 00:14:16.519 --> 00:14:20.080 transfrase or COMT, which is heavily located in the liver 248 00:14:20.159 --> 00:14:20.679 and tissues. 249 00:14:20.879 --> 00:14:24.399 So the monoamine oxidase enzyme isn't even the primary clearance 250 00:14:24.480 --> 00:14:27.320 mechanism for our local anesthetic. 251 00:14:26.840 --> 00:14:30.960 Exactly because the COMT pathway remains fully functional. The injected 252 00:14:31.000 --> 00:14:34.720 epinephrine is cleared efficiently and does not accumulate to toxic levels. 253 00:14:35.240 --> 00:14:39.399 Standardental local anesthetics with epinephrine are perfectly safe for these patients. 254 00:14:39.480 --> 00:14:41.039 That's a huge relief it is. 255 00:14:41.519 --> 00:14:45.240 However, the text explicitly warns that ephedrin, a different sympathy 256 00:14:45.240 --> 00:14:48.960 almometic sometimes used in emergency management, is a major risk. 257 00:14:49.279 --> 00:14:53.039 Ephedrin promotes the release of endogenous norbinefhrine from nerve terminals, 258 00:14:53.320 --> 00:14:56.000 which does rely on monoamine oxidase for breakdown. 259 00:14:56.200 --> 00:14:59.919 So administering ephedrine to an MAOI patient will cause that 260 00:15:00.120 --> 00:15:04.120 feared hypertensive crisis. But the lytokane with epinephrine in your 261 00:15:04.159 --> 00:15:08.279 syringe is metabolically safe. That is a critical distinction between 262 00:15:08.279 --> 00:15:10.840 exogenous administration and endogenous release. 263 00:15:11.000 --> 00:15:11.600 Very critical. 264 00:15:11.639 --> 00:15:14.279 All right, Let's examine the prescriptions we generate chair side 265 00:15:14.639 --> 00:15:19.720 ns ads and antibiotics. The dictionary lists several absolute contraindications 266 00:15:19.720 --> 00:15:23.759 for nsides like ibuprofen or neproxin. You cannot prescribe them 267 00:15:23.799 --> 00:15:29.000 to patients taking allandronic acid, systemic cortichosteroids, or sucral fate. 268 00:15:29.440 --> 00:15:33.120 Yeah, all three of those systemic medications inherently compromise the 269 00:15:33.159 --> 00:15:37.639 integrity of the gastrointestinal mucosa. NSAIDs function by inhibiting the 270 00:15:37.720 --> 00:15:42.799 cyclogenes enzymes, particularly kox one, which is responsible for synthesizing 271 00:15:42.840 --> 00:15:46.480 the protective prostic landins that maintain the stomach's mucosal barrier. 272 00:15:46.559 --> 00:15:48.080 So you combine them and its disaster. 273 00:15:48.200 --> 00:15:50.919 Right. When you combine an NSAID with abysphosphinit or a steroid, 274 00:15:50.919 --> 00:15:54.600 you completely strip away the gastric defenses, creating a synergistic 275 00:15:54.639 --> 00:15:59.720 catastrophic risk for severe peptic ulceration and massive gastrointestinal hemorrhage. 276 00:16:00.000 --> 00:16:03.399 When the prostaglandin inhibition isn't just a gastintestinal issue either, 277 00:16:04.080 --> 00:16:10.399 it heavily impacts renal hemodynamics. Nsais actively antagonize the hypotensive 278 00:16:10.399 --> 00:16:13.799 effects of blood pressure medications like methyl dopa and przosin. 279 00:16:14.120 --> 00:16:17.840 Yeah, the kidneys rely on those same prostaglandins to maintain 280 00:16:17.919 --> 00:16:23.320 renal blood flow and facilitate sodium excretion. By inhibiting prostaglandin synthesis, 281 00:16:23.639 --> 00:16:28.679 n sides cause renal vasoconstriction and sodium retention, directly counteracting 282 00:16:29.000 --> 00:16:32.759 the pharmacological mechanisms of the anti hypertensis. 283 00:16:32.039 --> 00:16:35.480 So you can significantly elevate a patient's blood pressure over 284 00:16:35.519 --> 00:16:38.600 the course of a few days, just by prescribing ibuprofen 285 00:16:38.679 --> 00:16:42.559 for post operative pains easily. What about the antibiotic cascades. 286 00:16:42.840 --> 00:16:46.840 We know tetracyclines are notoriously unstable in the gastriin testinal tract. 287 00:16:47.000 --> 00:16:50.080 They are highly susceptible to chellation. If a patient is 288 00:16:50.080 --> 00:16:53.799 taking aluminium hydroxide as a daily antacid, or a polysaccharide 289 00:16:53.840 --> 00:16:57.720 iron complex for anemia, the presence of those polyvalent medications 290 00:16:57.759 --> 00:16:59.720 in the gut is highly problematic. 291 00:16:59.840 --> 00:17:01.600 They bind together exactly. 292 00:17:01.799 --> 00:17:05.599 The tetracyclin molecules bind tightly to the aluminum or iron ions, 293 00:17:05.880 --> 00:17:10.519 forming massive insoluble complexes that just cannot cross the intestinal mucosa. 294 00:17:10.880 --> 00:17:13.759 The antibiotic absorption is completely integated, It passes through the 295 00:17:13.759 --> 00:17:18.640 GI tract unabsorbed, and your odontogenic infection continues to spread unhindered. 296 00:17:18.680 --> 00:17:21.799 Wow, And you know, if we're doing sedation, we have 297 00:17:21.880 --> 00:17:24.759 to look at metazolam and diazepam too. They rely heavily 298 00:17:24.759 --> 00:17:28.680 on hepatic clearance. The dictionary highlights severe interactions with drugs 299 00:17:28.680 --> 00:17:32.759 like verapamil, a calcium channel blocker, and rotonovir an HIV 300 00:17:32.880 --> 00:17:36.200 protase inhibitor. Now, a dentist might look at rotonovir, an 301 00:17:36.200 --> 00:17:39.519 antiviral drug, and assume it has absolutely zero overlap with 302 00:17:39.559 --> 00:17:41.000 the benzodiazepine sedative. 303 00:17:41.079 --> 00:17:43.119 You'd think so, but it comes down to the cytochrome 304 00:17:43.160 --> 00:17:46.000 P four fifty enzyme system in the liver. Specifically, the 305 00:17:46.000 --> 00:17:50.279 CYP three A four isoenzyme. Mitazoone is heavily dependent on 306 00:17:50.359 --> 00:17:53.759 CYP three A four for its metabolism and clearance from 307 00:17:53.759 --> 00:17:54.519 the bloodstream, and. 308 00:17:54.559 --> 00:17:56.599 Let me guess those drugs inhibit it. 309 00:17:56.720 --> 00:18:00.480 Both verapamil and rotonivir are potent inhibitors of that specific enzyme. 310 00:18:00.759 --> 00:18:03.440 If you administer a standard weight based dose of midazolam 311 00:18:03.480 --> 00:18:06.759 to a patient on retonivir, the livers simply cannot process it. 312 00:18:07.039 --> 00:18:10.559 So the sedative effects doesn't just last longer, it compounds. 313 00:18:10.960 --> 00:18:17.200 The plasma concentration of midazolam skyrockets, leading to prolonged, profound 314 00:18:17.240 --> 00:18:21.680 sedation and a massive risk of severe respiratory depression. You 315 00:18:21.720 --> 00:18:24.000 are navigating blind if you don't account for a paddic 316 00:18:24.079 --> 00:18:24.839 enzyme inhibition. 317 00:18:24.920 --> 00:18:26.240 So what's the protocol there? 318 00:18:26.559 --> 00:18:30.319 The clinical protocol mandates drastically lowered doses of the sedative 319 00:18:30.759 --> 00:18:36.319 titrated incredibly slowly with continuous pulse oxymmetry and cabnography monitoring. 320 00:18:36.799 --> 00:18:39.720 That brings us perfectly to the logistical reality of treating 321 00:18:39.720 --> 00:18:44.319 these patients. How do these complex pharmacological profiles dictate the 322 00:18:44.319 --> 00:18:48.599 physical chair side management? Let's analyze the diabetic patient. We're 323 00:18:48.599 --> 00:18:53.359 looking at oral antidiabetics, sulfonylurias like libin chlamide, or big 324 00:18:53.359 --> 00:18:57.079 one eyes like met Foreman. The primary acute threat during 325 00:18:57.079 --> 00:19:00.359 a dental appointment is a hypoglycemic crisis right ll Yes. 326 00:19:00.640 --> 00:19:04.279 Dental anxiety often completely disrupts a patient's routine. They skip 327 00:19:04.319 --> 00:19:07.039 breakfast because they're nervous or because they mistakenly believe they 328 00:19:07.079 --> 00:19:09.200 need an empty stomach for a local anisset of procedure, 329 00:19:09.279 --> 00:19:12.839 but they still take their glibin comide, Their endogenous insulin spikes, 330 00:19:12.960 --> 00:19:16.200 the LOGOS drops, and they crash in the chair. The 331 00:19:16.240 --> 00:19:19.240 logistical management requires scheduling these patients in the early to 332 00:19:19.279 --> 00:19:22.720 mid morning, during the most stable phase of their glycemic cycle, 333 00:19:23.160 --> 00:19:26.920 verifying chlored intake before ever reclining the chair, and having 334 00:19:27.160 --> 00:19:29.440 oral glucose gells immediately accessible. 335 00:19:29.480 --> 00:19:33.559 But the dictionary points out something wild. Our own prescriptions 336 00:19:33.559 --> 00:19:38.079 can actively manipulate their glycemic control. High dose aspirin and 337 00:19:38.160 --> 00:19:43.000 certain enosides can actually induce hypoglycemia in patients taking sulfonuluria. 338 00:19:43.039 --> 00:19:46.279 Yeah nisides are highly protein bound in the plasma. They 339 00:19:46.319 --> 00:19:50.559 can physically displace the sulfonilaria molecules from the plasma proteins. 340 00:19:50.119 --> 00:19:52.000 So it makes the diabetic drug stronger. 341 00:19:52.200 --> 00:19:55.160 This sudden increase in the unbound active fraction of the 342 00:19:55.200 --> 00:19:59.319 diabetic drug artificially amplifies its effect, driving the blood glucose 343 00:19:59.359 --> 00:20:03.400 down danger low WOW. Conversely, if you prescribe a short 344 00:20:03.440 --> 00:20:07.480 course of corticosteroids to manage severe post operative edema, steroids 345 00:20:07.519 --> 00:20:13.240 stimulate gluconeogenesis and induce peripheral insulin resistance. They aggressively antagonize 346 00:20:13.240 --> 00:20:16.960 the diabetic medication, causing a sharp spike in hyperglycemia. You 347 00:20:17.000 --> 00:20:18.960 cannot prescribe blindly in the population. 348 00:20:19.319 --> 00:20:22.480 Let's apply that same logistical scrutiny to the respiratory patient 349 00:20:23.119 --> 00:20:27.240 someone presenting with severe asthma or COPD managed with broncho 350 00:20:27.279 --> 00:20:32.319 dilators like aminofolline or sealbutamol. From a purely mechanical standpoint, 351 00:20:32.319 --> 00:20:33.759 positioning is critical. 352 00:20:34.000 --> 00:20:36.880 Very you must avoid placing these patients in a fully 353 00:20:36.880 --> 00:20:40.720 supline position. When they are laid flat, the adominal viscera 354 00:20:40.799 --> 00:20:41.720 compress against the. 355 00:20:41.680 --> 00:20:43.759 Diaphragm, which makes breathing harder. 356 00:20:44.160 --> 00:20:47.279 For a patient whose forced expiratory volume is already severely 357 00:20:47.279 --> 00:20:52.039 compromised by broncho constriction or alveolar degradation, that mechanical pressure 358 00:20:52.079 --> 00:20:56.039 against the diaphragm can rapidly induce respiratory distress. You have 359 00:20:56.079 --> 00:20:58.680 to maintain them in a semi supine or upright position 360 00:20:58.960 --> 00:21:01.559 to allow maximum diaphramatic excursion. 361 00:21:01.799 --> 00:21:05.640 The dictionary also highlights two significant chemical triggers for asthmatics 362 00:21:05.680 --> 00:21:09.680 that we utilize constantly. First, a well documented cross reactivity 363 00:21:09.839 --> 00:21:13.039 or a significant percentage of asthmatic patients possess an intrinsic 364 00:21:13.119 --> 00:21:18.119 allergy to aspirin, which can precipitate an immediate severe bronchospasm. Second, 365 00:21:18.400 --> 00:21:22.119 the hidden trap in our local anesthetic cartridges sulfite preservatives. 366 00:21:22.319 --> 00:21:25.599 This is a huge one. Epinephrine is highly unstable and 367 00:21:25.680 --> 00:21:31.000 oxidizes rapidly. To prevent this, manufacturers add sodium metabosulfite to 368 00:21:31.039 --> 00:21:35.359 any local anesthetic cartridge containing a vasoconstrictor O. A subset 369 00:21:35.400 --> 00:21:39.079 of asthmatic patients are severely allergic to these sulfide preservatives, 370 00:21:39.960 --> 00:21:42.799 So the very injection you are using to achieve profound 371 00:21:42.799 --> 00:21:46.720 anesthesia could instantly trigger a severe asthmatic crisis. 372 00:21:46.759 --> 00:21:47.759 So what's the workaround? 373 00:21:47.880 --> 00:21:50.759 If they have a known sulfite allergy? You are restricted 374 00:21:50.759 --> 00:21:55.519 to using plain local anesthetics without epinephrine like three percent mapivacane, 375 00:21:56.079 --> 00:21:59.960 which dramatically reduces your working time and eliminates surgical heat. 376 00:22:00.119 --> 00:22:03.480 Mosttases and additionally, the physical tools we use can compromise 377 00:22:03.559 --> 00:22:06.599 their airway. Placing a rubber dam is the standard of 378 00:22:06.640 --> 00:22:10.400 care for ENDO and restorative isolation, but it completely includes 379 00:22:10.440 --> 00:22:13.519 the oral airway. For a severe asthmatic or a COPD 380 00:22:13.680 --> 00:22:16.960 patient who relies on accessory oral breathing, a rubber dam 381 00:22:17.000 --> 00:22:21.440 can severely embarrass their respiration. If isolation is non negotiable 382 00:22:21.480 --> 00:22:25.480 for the procedure, the protocol mandates providing supplemental oxygen via 383 00:22:25.640 --> 00:22:28.720 a nasal canula throughout the entire appointment to maintain their 384 00:22:28.720 --> 00:22:30.200 oxygen saturation. 385 00:22:30.200 --> 00:22:35.359 And Logistical management is also about infection control, particularly with tuberculosis. 386 00:22:36.319 --> 00:22:39.640 If a patient's medical history reveals active TB, management with 387 00:22:39.720 --> 00:22:45.000 drugs like if ambatol isoni acid or rafambitsin the protocol 388 00:22:45.079 --> 00:22:48.799 is absolute. Elective dental care is strictly contraindicated. 389 00:22:48.880 --> 00:22:51.960 You postpone everything until they are medically cleared. But they 390 00:22:52.000 --> 00:22:56.920 present with an acute dental emergency like a severe facial 391 00:22:56.960 --> 00:22:59.960 swelling or intractable pain, you're obligated to tree. 392 00:23:00.359 --> 00:23:03.839 In that emergency scenario. You have to manage the aerosolization risk. 393 00:23:04.279 --> 00:23:07.000 The high speed hand piece and ultrasonic scaler create a 394 00:23:07.039 --> 00:23:10.799 massive aerosol cloud that can easily disseminate the mycobacteria throughout 395 00:23:10.839 --> 00:23:13.680 the operatory. Right, you must utilize a rubber dam to 396 00:23:13.759 --> 00:23:16.640 isolate the operating field from the pulmonary tract, assuming their 397 00:23:16.680 --> 00:23:19.880 airway can tolerate it and operate under high volume evacuation 398 00:23:20.200 --> 00:23:23.359 with full N ninety five particulate respirators and fee shields. 399 00:23:23.559 --> 00:23:26.720 We've mapped out a massive amount of pharmacological data today 400 00:23:27.079 --> 00:23:31.839 from receptor pathways to hepatic enzyme inhibition. So to solidify 401 00:23:31.880 --> 00:23:34.519