too. So, Berenice, are you going to tape? Yes, I've started recording. Okay, great. Yep, our second night. So, tonight we have Dr. Meyer, who will be covering the clinical occupational medicine two and three, and obviously any other questions. So, it's probably easier if you have a question to perhaps either raise your hand, or you can go ahead and type it in the chat box, and I can help monitor that too. Yeah, okay. Yeah, because that shows up for me too. So, excuse me. Yeah, so, any comments on the course so far? Looks like it's been going for a couple of days. Anything that's not clear? First, you know, sort of three, first three, four lectures. Once you've kind of gotten through those, you're through like the really densest part of the course, and the only really big clinical section that you have, aside from this, is the pulmonary one, which I think is the seventh module in the group there, and so that'll be the other big one there. But yeah, so what these modules, with the one Francesca did yesterday, and these ones, which are really the absolute meat of occupational medicine with the musculoskeletal skin disorders and the like, are all sort of fair game. So, anybody can either raise their hand, or type into the group chat, which I can see, or comments, questions. Anybody want to comment on how it's going so far? Anything like that? Otherwise, we'll jump over to the questions, and at least try and do them in a way that kind of emphasizes, not only, I like to sort of cover why all the wrong answers are wrong, in addition to that. So, but anybody, anybody have any commentary? And remember to unmute yourself if you're trying to ask a question, or raise your hand, and otherwise type into the group chat, and otherwise, if that doesn't work, I'll try pulling up the slides for questions. So, I'll just give everybody a minute, if they need to compose themselves. All right, a couple more people logging on. Anybody? Okay, well, I'm hoping that, hoping that, what's the best words to utilize this slide information, in terms of guiding what to study? That's sort of an interesting question. So, in guiding what to study, I think what we've done is, it's a good question, because this is the sort of thing that we sort of speak about, but doesn't come across as well in the slides so much. But I think what we've done is, tried to cover the information that presents on the ABPM guide for study. So, if you go to the website for the American Board of Preventive Medicine, you can download the outline, and the, you know, fundamentally, they've come up with an outline of what you should know. And what we've done is, tried to follow that. And so, the length of material is generally kind of a good emphasis on what they will be asking. So, that's why we cover musculoskeletal fairly hard. That was probably about an, you know, a bit over an hour's worth of lecture for us here. By the same token, pulmonary, in the next couple of days, will be much the same. And some of the other things, we kind of put in a little bit more glancing. But I think the slide information, we'll sort of see that, because we've kind of constructed the questions to work around how the boards work, and what sort of questions they're going to ask, and what we're emphasizing. So, I think between the slides, and then going off to the study questions, we'll see a little bit more about how those work, and what sort of information people want on it. So, hopefully, that answers the question we just got here. Anybody else? Raise their hand. Anything like that? Speaking? Typing? Group chat? Otherwise, we'll kind of move on to the questions. And so, let's pull up the same sort of questions that I'm hoping that everybody did. If not, we'll... So, let's find this, and share that. And let's see if I can go to a full view, because that'll help us. And it may not work. Come on. Let's see how else I can do that. Bear with me a second here. Page width. So, what we'll do instead is collapse the ribbon. And instead, so that won't be 100% view, but we'll do that. And so, okay. So, and there's a little bit, a little less nicely than we can manage it at the, during the course of the live course itself. But we'll just, we'll try and cover these answers, and I'll talk about it there. Unfortunately, people can't sort of shout out or yell out the answers for this here. So, anyway. So, let's look at the review questions for musculoskeletal disorders. And what we see is, and people can sort of log on to the chat if they don't get it here. So, first question, NIOSH lifting recommendations to prevent back pain include which one of the following? So, let's look at the answers here. So, do the NIOSH lifting recommendations try to get you to avoid lifting more than 25 pounds? Well, sort of thinking about that a little bit. Commerce, or at least UPS and Amazon would grind to a halt if you couldn't lift more than 25 pounds. And most people can reasonably be expected to lift 25 pounds. So, that's probably not the answer there. It's heavier weights than most. Second question, using back supports. And just brief question, does NIOSH let you use back supports or endorse back supports? And the answer there is also no. And I think I mentioned that you see those get used in places like the DIY stores. And, you know, again, I tend to think that they form a little bit of a string around people's fingers if you're wearing them. When you're doing a lot of lifting, it keeps you from bending down at the back. And so, if you feel this on your back, you might be more inclined to say, oh, yes, right, I have to lift from my knees and then squat down. But back supports, there's no evidence that they're either preventive for back pain or that they're good for treating it. Avoid twisting or bending during lifting. So, yes. So, avoidance of that includes twisting or bending, puts torque generally on the lumbar area. And so, if you are twisting or bending during the lift, you not only have a lifting weight, but you're also supplying that much more torque to it. So, that can exacerbate or even cause back pain. And so, the correct answer there is C. And rapid lifting is, of course, not a lifting recommendation to prevent back pain. You want to be able to do it slower and more controlled. So, of those choices, you want to avoid twisting or bending during lift. And as I mentioned before, that would increase back pain. And because of the torque that it puts on the lumbar spine. Okay, good. So, stop, type in chat if you have any other questions. So, the second one, ACOM guidelines provide the strongest recommendation for which of the following initial treatments for a worker with new onset low back pain. So, here again, with the question, you're talking about initial treatments and new onset low back pain. So, the first time you see a patient, not necessarily farther on out when they might have developed some other problems. So, the potential answers here, epidural injections, and of course, probably not, certainly not, given the way the question is worded, which you're looking at initial treatments and new onset low back pain. So, that would be the, that would be the, excuse me a second, that would be the appropriate time there. So, there was one chat question about leveraging time and maybe I'll address that at the end while I still have people on here. Okay. So, epidurals injections are a later treatment. And if you have evidence of lumbar radiculopathy and somewhat farther on down the road, certainly you would give that about four to six weeks, at least, probably longer before even considering that. And post imaging is when you're going to decide on epidurals. So, second answer, nonsteroidal and inflammatory meds. And as you recall from the slides, yes, those are one of the real mainstays of treatment. So, nonsteroidals generally get in ACOM and other recommendations, get an A or a B level in favor of it, meaning that there's good evidence from adequate epidemiologic trials for nonsteroidals. And the second one, usually getting about a B recommendation are muscle relaxants. So, the combination or starting off with nonsteroidals plus minus muscle relaxants is going to be the best way of doing that. C, opioid analgesics. If you put that, given all that we know now and nowadays, if you wrote that opioid analgesics were the first line or initial treatment for that, better go back a little bit and work on that some more. So, clearly not one of the indications for opioid analgesics, not in uncomplicated low back pain. There has to be trauma, crush injury, tissue damage, broken bones, et cetera, et cetera, for opioid analgesics to be indicated. And again, sort of keeping it very much to a minimum of two weeks or thereabouts and with frequent checks on the worker. And bed rest, again, we kind of emphasized in the slides that bed rest is contraindicated in the bad old days. When I was a resident, it was actually given the first indication, you would say, go and rest it and come back in a week or 10 days or so of bed rest. And of course, that weakens the lumbar musculature and contributes to non-recovery fairly quickly. So, the main treatment, again, is being up and around. So, the answer for two is nonsteroidals. Moving on to three, which of the following presentations would lead you to diagnose a unilateral L4-5 lumbar disc? So, saddle anesthesia. So, where do we see saddle anesthesia is going to be generally in cauda equina syndrome. So, that leaves out the unilateral part of this questioning. Quadriceps weakness. This is going to be generally higher. So, the L4-5 disc is going to usually affect the L5 nerve root, possibly the L4, but usually the L5 root. So, quadriceps weakness is going to be up a little bit higher. Diminished ankle jerk. So, this gets into one of the sort of questions about reflexes, where the ankle jerk is generally an S1 reflex. And so, this wouldn't be seen at an L4-L5 lumbar disc herniation, where again, the probability is more of an L5 root there. So, the L5 root doesn't have, at least for the purposes of the boards and purposes of what we're studying for here, there's various shades of how it works there. But in broad brush general terms, and certainly for the purposes of the boards, an L4-5 lumbar disc is going to be too high for diminished ankle jerk, which would be an S1. And weakness on heel walking. So again, I like heel walking and toe walking because these are people trying to support their full body weight. And so, heel walking or weakness on heel walking is generally indicative of an L5 root lesion and weakness on toe walking, if they're unable to support themselves walking on tiptoe, that tends to at least indicate or implicate more of an S1 root. So, the answer here is actually D, the last one we're talking about. Okay. So, moving on here. Of the tests below, the most sensitive diagnostic criterion for carpal tunnel syndrome on history and physical examination is, so we'll dispense sort of A and B right away. So, Tunnell's and Phelan's. We use those all the time. We use them constantly. We're never going to get out from under using those. But if you recall or look back on the slides for it there, Tunnell's and Phelan's are somewhat sensitive and pretty nonspecific. And I think some of the sensitivities on, forget which one, I think probably Tunnell's sign ranges anywhere from 10% to 90%. So, you might as well flip a coin instead of actually doing the maneuver for all the sensitivity is worth. Now, we do them because there are signs of median nerve irritability, but they aren't reliable. They can indicate other things and you can, many of you may be able to actually reproduce a Tunnell's or even a Phelan's sign on yourself. So, they lack both real sensitivity and specificity. Workers' comp managers will want to see that you did them in your history and the like, but they're not fantastic. Katz-Hyden diagram is sort of interesting. There was a picture of one in the slides themselves, and that is generally for the worker or patient that you're seeing to indicate where they note numbness, tingling, paresthesias, pain, a variety of things that they can draw in. And it's fairly sensitive for carpal tunnel syndrome if they draw in the median nerve distribution. And so, that would be the palm of the hand and fingers, thumb, index, and middle finger, plus minus splitting the fourth down the middle. And of course, the pinky and the ulnar side of the fourth finger are instead innervated by the ulnar nerve. So, Katz-Hyden diagram of these is going to be probably the most specific and sensitive because they sort of shaded in the areas where they do it. If they do the back of the hand, back of the arm, shade in the pinky, then you're probably not looking at carpal tunnel syndrome, but maybe looking at some other disorder. All right. And lastly is fifth finger abduction weakness. And so, I kind of mentioned this a little bit. Weakness in the fifth finger is going to be what the ulnar nerve innervates many of the intrinsic muscles of the hand, as opposed to the median nerve, which is really just innervating. It's only motor innervation is in the thenar eminence. So, the fifth finger is going to innervate many of the intrinsic, including the hypothenar muscles. So, if you have a patient who has weakness when you ask them to abduct their pinky finger against force, as I'm doing here, then that may be more related to ulnar neuropathy, probably cubital tunnel syndrome. All right. So, the answer there is the Katz-Hyden diagram, or number C. Parasthesias in the fourth and fifth finger and abductor digitae. Quinti weakness would prompt you to closely examine. Well, guess what? I gave you sort of the answer to this before, right? Because of number four, I just talked about fourth finger abduction weakness. So, that's the ADQ or AD5 weakness. Parasthesias in the fourth and fifth finger, we mentioned again, are related to the ulnar nerve. Now, of these choices, let's say we can right away then eliminate B, because we know it's not carpal tunnel syndrome, because it's not a median neuropathy. And we can eliminate pronatory teres syndrome by the same token, which is a median neuropathy farther up in the arm near the antecubital fossa. So, that leaves us with A and C, Guion's canal and the cubital tunnel. And of the two, Guion's canal is the tunnel in which the ulnar nerve and the ulnar artery pass through the wrist. And compared to the carpal tunnel, which has all the flexor muscles of the hand, all the extrinsic flexor muscles of the hand pass through the carpal tunnel syndrome, pass through the carpal tunnel. So, that's rather full. Guion's canal is rather capacious. There's very little passing through it other than the ulnar nerve and artery. And so, people tend, it's not 100%, but if you wanted to put money on it, Guion's canal is not where it's happening, because the ulnar nerve does have room to move, and it doesn't get compressed in that canal. So, the answer here is the cubital tunnel up in the elbow, which is a flexor joint. The elbow has a fairly good range of motion, both in supination pronation and flexion extension. And people are going to use, in this case, the flexors of the hand and wrist that originate from the elbow also. So, more likely, if you see evidence of an ulnar neuropathy, that's going to be related to an entrapment in the cubital tunnel. All right. So, we're going to kind of move on to skin disorders here. And chloracne, it would be seen in workers who recycle or dispose of electrical equipment from exposure to, and first question is arsenic. And so, arsenic is generally not a component of electrical equipment. So, that's one strike against it. And the second point is that it doesn't cause chloracne. So, what is arsenic cause? If you're thinking specifically about skin disorders, arsenic, you want to think hyperpigmentation. So, keratosis, hyperpigmentation, oftentimes big keratotic plaques, and subsequently down the road leading to squamous cell carcinoma of the skin. By contrast, PCBs, so PCBs and dioxins, which are multiple halogenated, mainly chlorinated, aromatic organic compounds are most associated with chloracne. And so, PCBs were used as liquid insulators in a variety of electrical equipment, particularly those really big transformers that you see around electrical transforming stations. Dioxins being the other compound that causes chloracne, and that was a contaminant, generally a contaminant of things like Agent Orange and herbicides. So, the answer here is PCBs. Acrylates will give people a rash and skin desquamation. So, again, not chloracne. And carbon disulfide tends not to have many effects on the skin. We'll see when we get to the cardiac lectures, what that tends to do and all the nasty things that happens. Okay. So, moving on. Fiberglass canoe maker develops a rash over forearms and shins. And so, this is very common. Many people come into contact with fiberglass, may develop this sort of rash. So, the most likely diagnosis would be, would be A, allergic contact dermatitis. Pretty rare. Fiberglass is very inert. It tends not to be allergenic because mainly sort of just glass fibers. And that is something people tend, very unusual if not at all, to be allergic to. Irritant contact dermatitis. Yes, so by contrast with allergic contact dermatitis, so glass isn't an allergen, but it's an irritant, and the form in which fiberglass comes, which are these sort of small threads, spicules and the like, tends to get on the skin, get embedded oftentimes in the skin, poke through the outer layers of the epidermis, and causes just a straightforward irritant reaction in the skin. And the latter two, IgE urticaria, again, thinking here, itching maybe, but you're not gonna have the manifestations of urticaria as you would in, for example, latex urticaria or other reactions that cause wheel and flares. You're not gonna see indurated skin with erythema, and the abrupt severe itching, it'll be more long-term chronic and probably milder than urticaria. And photodermatitis really doesn't, again, not very reactive material since the main compound is glass, so it's not likely to cause a photodermatitis. So here we're looking at kind of a classic irritant contact dermatitis from fiberglass. Okay, rounding out this one here. I think we're keeping on time. You should be suspicious of an occupational cause for squamous cell skin cancer that arises in indoor workers. So if somebody works in an office building and has all their life, they work in offices, work in laboratories, something along those lines. And of course, recreational sun exposure is another factor in causing squamous cell cancer. But if you have a strictly indoor worker, and especially of a younger indoor worker, you might be more suspicious of an occupational cause than you might be for just pure sunlight. You should be doubly suspicious if this cancer is in an area that's not normally sun exposed. So if you see it on the buttocks, for example, particularly in a male, or the lower back or areas that are generally clothed, it's not a sort of a complete hard and fast rule, but if you are seeing that in non-normally sun exposed areas then you're sort of putting two and two together, they're not particularly at risk for sun induced skin cancer and it's not on a sun exposed area. So you might wanna take an occupational history and here the question is focusing on exposure to something that would cause squamous cell skin cancer. And so of these choices here, the first one, again, I kind of mentioned it early on in the talk here, but I'll mention it again here is arsenic. So arsenic runs the gamut from hyperpigmented lesions to keratotic lesions to what's called Bowen's disease or squamous cell carcinoma in situ in the skin. In other words, before it's become invasive on down to invasive squamous cell skin cancer, squamous cell cancer skin. Dioxins don't necessarily cause that, they can cause other cancers in particular that are associated with non-Hodgkin's lymphoma and with soft tissue sarcomas, but not with skin cancers, certainly not squamous cell skin cancers. Mercury is not really a carcinogen, I don't know of anything where it's sort of rated as clearly causing cancers. And thallium was used as a rat poison, it's banned in the US there, but in general it causes neuropathic symptoms with alopecia, some falling out of hair. So oftentimes can get mistaken for radiation exposure. So the answer here, as it alluded to in an earlier question is arsenic. And lastly, your suspicion for an allergic contact, occupational contact dermatitis increases. So now we're again suspicious of it when you find that your worker has an AGE or an atopy. So what's sort of interesting in this, is a trivia question that goes way back to the boards when I was a resident here was that atopics were found the opposite of what you might expect. Atopics were found to develop a higher incidence of irritant contact dermatitis. And back when I was a resident, the cause wasn't elaborated, but basically it's a functional mutation and what's called the phylagrin gene, which is responsible for dermal connectivity and integrity. And so oftentimes even without irritant contact dermatitis, sometimes the people who have atopics may have sort of xerotic skin. So remember that allergic contact dermatitis is not a IGE mediated immunity. In any case, it's a type four or delayed hypersensitivity reaction. Okay, so it's not A, the rash or lesion demonstrates sharply demarcated borders. Now that's also another potential sign of irritant contact dermatitis because irritant contact dermatitis only irritates the skin in the areas where it's in contact with the skin. There's no extension beyond it. You might have a little bit of a reaction, sure, but really the basic take-home message is you get irritant contact dermatitis on areas of the skin where you come in contact with, as opposed to potentially allergic contact dermatitis where, again, it's a type four allergy and you might have systemic manifestations or it may spread, which again, is probably familiar to many of you from seeing poison ivy cases and would imagine with your poison ivy cases that many of you have seen people who've come back and complained that it was spreading, quote-unquote, and they go and wash their clothes off, you blame the dog, whatever else, and what you're really seeing is actually just systemic manifestations of it going beyond the areas like their hands or the feet where they came into contact with it. All right, so we've rolled out the first two there. You find out the majority of your patients' co-workers have the same problem. Well, that also is more indicative of an irritant contact dermatitis, so that's another point for irritant here, is that irritants are going to universally irritate a lot of workers. Not everybody will have an irritant contact dermatitis, but more than one person or just a couple of people will have an irritant contact dermatitis if there's an irritant in widespread use because it just wreaks its damage on the skin, so to speak, whereas, by contrast, allergic contact dermatitis, because it's idiosyncratic, you have to develop an allergy-slash-sensitization to that. Oftentimes, just a few workers, even if the material's in fairly widespread use, oftentimes, maybe just a few workers will develop dermatitis, and so, D, the rash seems to persist and even worsens despite removal from the workplace, and that is a sign of suspicion for an allergic contact dermatitis, and with many allergens, and so this goes both for skin disease and oftentimes respiratory disease, people may come into contact with that material when they're outside of the workplace because it's in common use outside, so that oftentimes doesn't occur for specialized solvents, metals, or other compounds that get used in the workplace, but many people develop allergies to things that are relatively common in the outside world, and just as an example, I had a delivery worker for one of the big delivery companies, delivery truck that goes out and delivers your packages from Amazon and everywhere else, and he developed an allergic contact dermatitis, so fundamentally all over his hands and arms, and he was eventually patch tested by the dermatologist. He had an allergy to colophony, so he had ACD related to colophony, and went out of work, and he improved out of work, but he never really did get better, and one of the reasons is because colophony as a natural product is used in a lot of paper products. It turns out for UPS, a lot of the coating for brown box packages and the tapes that are used have colophony on it along the outside as a coating, and in fact, many things in the home, including brown cardboard boxes, but also paper and other things use colophony as a coating as well, so that many workers can still, their dermatitis may still not go away despite removal from the workplace. Okay, any questions on here? I'm gonna sort of hold off a minute here. I know there was one chat question, and I'll try and sort of address that more towards the end of the show here also, so any questions, anybody wanna hit chat, or otherwise, I'm gonna move on to the second set of questions here. Close that. Okay. Just get that, and so I see about 19 or 20 people here, so let me just share the screen with the, so here is tab five, and let me just shrink this down again, collapse the ribbon here. How many questions do I have? Quite a few more here. All right. So these are the questions for clinical OCMED-3, which was something of a big grab bag of pulmonary toxicology, plus some other toxicologic things that don't fit very well into other aspects of the course, other than toxicology. So question one, which of the following is the major determinant of the type of respiratory symptoms after an irritant gas exposure? So starting off with A, water solubility of the gas, and so that is actually the main determinant of respiratory symptoms, and for the boards, what you wanna do is kind of split in your head which ones are water-soluble versus the ones that are non-polar, less water-soluble. The more water-soluble, more irritant, the more water-soluble, more aqueous ones, basically acids, acid mists, ammonia, chlorine gas is sort of an intermediate, but anything that would be polar or dissolve in water relatively easily, particularly acid, strong acids or strong bases are gonna cause upper respiratory type symptoms, at least till they get very, very high doses, in which case they get deeper, and there's a lot more in there, but basically the way to think about this again is nose, throat, oropharynx, nasopharynx, larynx, upper trachea for the water-soluble gases, and for the insoluble gases or less-soluble gases, namely phosgene, oxides of nitrogen, and to some extent hydrogen sulfide. Well, hydrogen sulfide's really an asphyxiant, so really what you wanna remember is phosgene, phosgene, ozone, and oxides of nitrogen are going to get deeper into the bronchoalveolar tree and even into the alveoli and cause their damage to the lung parenchyma. All right, quickly through the other choices, particle size, well, that's not a component of gas in any case, so that wouldn't be there. Frequency of exposure might be, but it's not really the main determinant there, so the main determinant, if you're frequently exposed, again, the main determinant is gonna be water solubility, and in this case, there's no real sort of intrinsic susceptibility. There are severe irritant gases. You can think of them by analogy with irritant dermatitis, and so intrinsic susceptibility matters much less, so the answer there is A. All of the following could stem from fermenting hay on a farm, and this is just to tell you that farming, as you probably gathered from initially these lectures and then later on when you hit the pulmonary lecture, is going to be a dangerous job, so all the following could stem from fermenting hay on a farm except for delayed acute lung injury, and so that can arise from a farm, so those are gonna be oxides of nitrogen coming from silo, which is silo-fillers disease, which is choice B, so those two are one in the same, release of highly water-soluble gases, so that is the one, or that answer is not correct, or it's the correct answer to the question, which is to get you to pick the except one, and that is because oxides of nitrogen are nonpolar or much less water-soluble and therefore penetrate deeply into the lung and the parenchyma, and increased incidence of respiratory illness from chronic low-level exposure, so the low-level exposed may develop reactive airways dysfunction syndrome, irritant asthma. If they get a big dose of it, one of their sequelae might also be bronchiolitis obliterans from the constant irritation and subsequent airway remodeling, so the answer here is the one that it's not, which is release of highly water-soluble gases. All right, carbon monoxide exposure, so when do we see carbon monoxide exposure? If I told you to go out and get carbon monoxide exposure, you'd run something hot, combustible fuel indoors there, so does that happen in the warm weather months? No, it doesn't really, so carbon monoxide is going to happen in November and onward, that is when people shut their doors, that's when the loading dock shuts its doors and starts running around those propane-fired trucks or the trucks park up close to the loading dock and run their exhausts for warmth, and suddenly in August, where you wouldn't have it in nice ventilation because everything's open, suddenly in November, you have a big buildup of carbon monoxide because the shed or loading dock is now closed. All right, so it occurs in the colder months. Is it excessive if carboxyhemoglobin levels are greater than 5% in a nonsmoker? And so, yes, that's accurate, so people, depending on where they are and not working around carbon monoxide are gonna have carboxyhemoglobin levels of about a percent or so, depending city versus rural traffic, et cetera, et cetera. If they're greater than 5%, it's clear that there's excessive carbon monoxide exposure. The level of symptoms may vary depending on age, smoking history, cardiac history, et cetera, et cetera, but it's clearly excessive if it's greater than 5%. Often presents with cherry red faces, that's sort of classic textbook carbon monoxide poisoning from second year medical school, pathology and physiology. The toxicologists tell me that they've never really seen that, and so I think I quoted a sort of a 2% presentation of it with cherry red faces. So it's supposed to be the classic, but you really don't see it in the case of carbon monoxide poison very often. You don't remember it, but it's not the be all and end all. And as a simple asphyxiant acts by displacing oxygen from the ambient atmosphere breathing zone. So here's the difference between simple asphyxiants and chemical asphyxiants. The simple asphyxiants just displace oxygen. So if I were to sort of fill the room with nitrogen or carbon dioxide, if I'm a minor and I hit a pocket of carbon dioxide or methane and it sort of spreads in this enclosed area, that's taking down the ambient oxygen level from 20, 21% down to 15 or 12% or something like that. So that's just simple asphyxia that's displacing oxygen from the air. Carbon monoxide doesn't do that. At smaller doses, you can still have an adequate oxygen in the ambient atmosphere, but carbon monoxide is going to attach to hemoglobin and become fundamentally a chemical asphyxiant rather than a simple asphyxiant. So it's not displacing ambient oxygen, it's latching onto hemoglobin and increasing the ability or the rate of reluctance of hemoglobin to give up oxygen in low or hypoxemic tissues. Okay, chemical asphyxiants. So here we are back in the chemical asphyxiants commonly arising from fecal matter and manure. So it's going to really stink. So it will be recognized by a rotten egg odor. Will it result in primary irritant symptoms? So no, this is the fecal matter and manure and the rotten egg odor should send up a signal that we're looking at hydrogen sulfide, H2S, and these aren't irritant symptoms. These are going to be chemical asphyxiants similar to, more similar to cyanide than anything else because it interferes with cellular respiration at the mitochondrial level. Will it injure farmers when silos are cleared out? No, going back up here, that silo fillers disease and oxides of nitrogen, probably those probably don't smell good either, but it's not from fecal matter and manure. Fecal matter and manure in the farmer isn't from clearing out the silo. It's from pumping out the manure pit and that's where the farmer's going to disrupt the manure and perhaps stir up hydrogen sulfide that's sitting on the surface of it. So it's just where you get cattle knockdowns. Also a by-product of metallurgy or smelting. So not again from fecal matter and the like. So this is going to be arsenic instead of H2S. So principally it's got that rotten egg odor, a chemical asphyxiant and very fast acting. So you can get knocked down, as I mentioned, knocked down of cattle, but also of people who get exposed to it in sewage and the like. Okay, moving on. So we've got pesticides here and recall how much I mentioned this in it here, but some places, particularly California, requires surveillance exams for pesticide applicators. And in many cases, pesticide applicators are going to be farm workers. And so this is one of the few protections in the workplace that many agricultural workers and particularly migrant workers have for their workplace. So California mandates that you get pre-application cholinesterase levels on workers before they go out and start to spread or apply organophosphate pesticides. So a few little factoids for that. They're decreased plasma cholinesterase may occur from a variety of drugs and medical conditions. That's true. Plasma cholinesterase is sensitive to a whole lot of problems, medicines that people take, liver disease, renal disorders and the like. So it's generally better to do red cell cholinesterase testing in those cases. And by the same token, B, red cell cholinesterase is a better reflection of CNS or nervous system effects. And that is actually also true. And C, plasma cholinesterase falls first, but red cell cholinesterase stays depressed longer. So the bottom line here is that if you're doing surveillance exams, red cell cholinesterase is a better reflection of CNS levels of poisoning. And by a similar token, plasma cholinesterase is affected by medicines, liver metabolism and the like. So the answer here is all of the above. Okay, characteristics of organochlorine pesticides. So ask yourself, I'll stop for a minute because I can't get people to sort of shout out answers here but organochlorine pesticides are things like DDT is sort of the most famous of the organochlorine pesticide was banned for a very long time and it's coming back in limited use. So they're usually fat soluble, so that's true. They accumulate in fat and the reason that they were problematic of a silent spring was that they were fat soluble and then they would accumulate on up the food chain so that they tended to accumulate in fish, predatory birds in particular ate fish and the predatory birds were getting as very bio-concentrated in the fish's fat and then concentrated in their own fat and that interfered particularly with bird reproduction, hence silent spring. So they're usually fat soluble. They may persist in environment, it should be environments and the body and slow metabolism. So yes, so they accumulate in fat, they're metabolized very slowly and they're environmentally persistent. I should probably change this there because C was, I guess they may still be used clinically. So briefly ask yourself again, where might you see organochlorine pesticides used? You don't apply DDT, but many of us, again, showing my age a little bit, may have prescribed lindane as a scabicide and other forms of a pesticide for people. So lindane is another organochlorine pesticide. It's use been kind of phased out clinically, especially, but not unique to children who might develop seizures as a result of lindane toxicity. So the answers here are all of the above, although I'd be willing to think that, because we really don't use lindane very much anymore, that A and B might be acceptable here. Okay, so you're trying to get rid of ants in your garden, you buy an ant poison from the neighborhood hardware store and you don't need an applicator's permit because it's got pretty low toxicity. Material has a low risk for health effects but when it does cause problems, its most frequent health effect is. And so here, it's a little bit mysterious and maybe the question's a little opaque, but here we're talking about pyrethrins and pyrethroids. You can actually go to the hardware store, the DIY store, the flower store, and buy ant poisons or sort of garden pest poisons without an applicator's permit. And for most part, majority of those pesticides are, excuse me, pyrethrins and pyrethroids. So what do they cause when they cause it? Not seizures, I think you'd have sort of tighter licensing or regulation for it if they did cause seizures. Allergic reactions, yes. So if you think pyrethrins think the most common problems they cause are skin, allergic contact dermatitis, sometimes asthma related symptoms, IgE type reactions as well. So maybe IgE or delayed type hypersensitivity reaction. Sweating and meiosis, not for these. If you see sweating and meiosis, you're gonna think of the mnemonic dumbbells and that is going to be a consequence of organophosphate, OP or carbamate poisoning. And delayed peripheral neuropathy is the other one you wanna remember from organophosphate poisonings is that causes this sort of immediate dumbbells type symptoms from acute poisoning, but high organophosphate, OP pesticide poisoning is going to potentially cause a delayed peripheral neuropathy some weeks after poisoning. Okay, moving around a little bit again, which of the following gases is not as simple as fixiant? So we've kind of been through those. So the three over here are going to just displace. Argon is particularly non-reactive because it's a noble gas. Propane and methane are explosive, but if you see them in mines, they're gonna be simple as fixiants because they don't necessarily cause the chemical type as fixia that for the three chemical as fixiants, you wanna think hydrogen sulfide, cyanide and carbon monoxide. So this is the one of those four that's not as simple as fixiant. OP pesticide poisoning may cause, does it cause salivation? Yes, so that's the S in dumbbells. Urinary retention, so that's the opposite of what it causes, right? Sort of opening up of everything, excretion and secretion from every pore and opening. So this is not what it causes. And along the same lines, diarrhea, yes. So salivation and diarrhea think pouring out. So the one it's not gonna cause is urinary retention. And so the answer there is A and C, which is the major determinant of potential toxicity of carbon nanoparticles. When carbon nanoparticles first came in, this was sort of a favorite board question of them, I think, not sure if they're still using it a lot, but we can have it on there. So based on that, what was the potential toxicity? Potential toxicity for it, our main determinant is particle size and surface to volume ratio increases the smaller and smaller a particle is. You have more surface for the volume that it's holding. And as a consequence, it can be more reactive with a high surface to volume ratio. Additionally, although not quite as clear, they start, they get small enough. So they start to kind of behave less in sort of classic particle physics. I shouldn't say particle physics and sort of classic Newtonian, just statics and motion. And they start to behave in sort of quantum mechanical ways and get more reactive that way. But in the main, they're particle size because they have more of a surface area to be reactive. And so they can react with small molecules and generate, for example, reactive oxygen species. And that's what causes their toxicity. So other things, fiber length, not as much as just particle size. Surface PAH concentration has been a concern in some cases for nanocarbon nanoparticles might contain because they're generally made from fossil fuels. So there's been a concern that they may contain polycyclic aromatic hydrocarbons. And so that's a concern, but not nearly the main determinant of their toxicity because some other ones may not have PAHs at all. And carbon valence is just gonna be the same no matter what, right? It's sort of simple organic chemistry. Okay, building related illness. I know everybody's favorite problem right now, but so one of the things you wanna sort of think about is how to sort of simplify problems, investigating buildings and not get sort of sucked into everybody's symptomatology. And so here are a few things to do or there's one thing to do anyway and many things not to do. So first answer, testing the patient's mold IgE titers and matching them to results of building sampling for mold. That is not the first initial approach you wanna do. It's what people tend to demand of you there. They're getting allergic symptoms or they're getting breathing or airway symptoms. They wanna be tested. So-and-so found this and that mold in the building, et cetera, et cetera. So they wanna get tested for the mold in the building. That is not the approach to take for trying to remedy the problems of the building. Answer B, the walkthrough with an industrial hygienist or a building scientist. That's the initial approach you wanna take with a building because you're looking for problems in the building because you're only going to remedy the workers slash patients problems in the building if you pay attention to what the potential sources are in the building. Look for water damage, look for a mold, use the grandmother test for mold, right? If your grandmother would point to it and say, that's mold, then that's mold. And you don't go crazy testing on it. You try and clean it up. You try and get the water damaged pieces out of the building. You clean up the mold, you find where the leaks are. You get all the fuzzy materials like old carpets and old furniture out of the building. So you walk through with an IH or building scientist. Third one, testing carbon monoxide in the building at various points in the day. That's something that you can do. It's probably not the first line of attack. And the other thing is this is slightly a trick question is that carbon dioxide is a good test of ventilation in a building. Carbon monoxide is not, it may point to a source of it, but you would also wanna be suspicious of that. Really only if people are getting carbon monoxide type symptoms, but carbon dioxide can build up in a building fairly readily. And that is a sign of poor ventilation as much as anything. You put out all these oxygen breathers, carbon dioxide generators in a building starting at eight or nine o'clock and at noon or one o'clock, suddenly the air is gonna be full of carbon dioxide. People are doing head dives at their desk. Everybody's headachy and irritable. And lastly, advising the patient to move to Arizona. That's, I'm gonna put it, that would be a joke if it didn't happen or I hadn't seen it happen in some other cases with some of the clinical ecologists. So clearly not the answer. And so the answer is a walkthrough with an IH or building scientist to determine that. Okay, so we're sort of finishing up. We've got mostly some matching questions here. All these lovely liver and kidney disorders, which are hard to sort of see or find to match the following terms. So beta-naphthalene. So many of these aromatic compounds you want to associate with bladder cancer. Remember that it started in the dye industry with aromatic amines. And so many of the similar type of compounds, aromatic hydrocarbons and aromatic amines are gonna be associated with bladder cancer. Vinyl chloride. That's one of the classics here. So that's associated with hepatic angiosarcoma. Very few things are causing hepatic angiosarcoma and vinyl chloride. Monomer, which is the monomer basic building unit for making polyvinyl chloride or PVC is associated with hepatic angiosarcoma. Methylenedianiline, MDA. This is a real sort of zebra that's responsible for cholestasis. Epingeondys flower was contaminated with MDA. Trichloroethylene, sort of one of the great fancy ones that works like antabuse or disulfiram. So you get this disulfiram reaction and that causes degreasers flush at all. So they may get it on their own or they may notice it with alcohol along with the flush, along with some of the other unpleasant consequences of disulfiram when you take it with alcohol. Will be characteristic of TCE. And of course it's being used by degreasers. And dimethylformamide, another one of these sort of more zebra type things there. This is used to making epoxy resins and that causes microsteatosis. What do you really want to remember out of that group? Want to remember beta-naphthalene, aromatics causing bladder cancer, vinyl chloride clearly with angiosarcoma and TCE for degreasers flush, just because many of those chlorinated hydrocarbons still in use. Solvents that cause steatosis. We all know about ethyl alcohol and yes, it does. So, and certainly carbon tetrachloride does. So that's going to be in all of the above. Enough said on that there. Most solvents are going to cause or can cause steatosis and liver damage by that mechanism. All right. So lastly is a short question on renal. And here's a few points you want to remember. Cadmium. So what is cadmium going to cause? Cadmium is associated with this metallothionein complex. So what it does, it gets absorbed, it gets transported to the liver. In the liver, it induces this protein called metallothionein, which complexes to cadmium. They hook up, they go to the kidney, they get deposited in the cytoplasm of the renal tubules, gradually leach out and poison the renal tubules, proximal renal tubules. So it's associated with this metallothionein complex. Mercury affects the glomeruli more than the proximal tubules. So you get a membranous glomerulonephritis. Solvents in broad brush general terms associated with Goodpasture's syndrome. Many of them might and some elaboration of IgA. And the other one you're going to want to remember is lead, which is associated because of its renal toxicity is associated with gout. So lead, think renal damage, think hypertension, think gout, think chronic renal disease or disorders. Okay, so I'm going to sort of put this one away here or I'll just kind of broaden this out here. Let's see if we can find who's still, everybody's still awake. Anybody still have any, so there was, let's see what we have for, we've got a few minutes to answer chat room. So somebody asked, any advice on how learners can best manage their time over the next few months to prepare for the upcoming exam? Is there a particular order that one should tackle? How many hours, roughly a day or week? Trying to get organized and that kind of thing. So some of the answers are sort of provided in the written material that I put at the very front of the chapter in Reader and that should also be available on the syllabus along either with the slides or the written material. But some of it is somewhat dependent on, I hate to say sort of the short answer is that it depends but there's a lot of different ways to go about it there. And first off, I think mainly is sort of recognizing the things that you know and recognizing the things you don't know. And in occupational medicine residencies in particular and even more so occupational medicine practice for those of you who are taking the recertifying exam is very individualized. It's very idiosyncratic. It's not like internal medicine or pediatric programs where everybody sort of gets a run of very similar diseases and disorders. Oftentimes there's a specialty of the house and my own program included. So you get to see a lot of musculoskeletal disorders in one program, a lot of pulmonary in another and neither of the other one at the other program. So I think maybe the first thing to do is sort of, take this course, go through the slides, identify what you know, what you really know well and what you don't know, and then sort of put your focus on the things that you don't know. You can kind of very much quickly brush up if you do a lot of musculoskeletal work or your residency has emphasized that, then great, that may not be something you have to worry too much about there. By contrast, if you haven't seen a lot of pulmonary disorders, if you haven't seen, if you haven't seen say commercial driver's exams or drug testing, you don't have to know those really in depth, but you wanna know some of the fundamental basics that Francesca covers in there. And so all of that, I think goes to sort of a first pass about how you go about studying it there and then focus on what you, leave aside what you do know, quickly brush up on that. You can do that at the end, but using this course and using the ABPM outline and whatever else you do, figure out from all of this what you haven't had experience at, what you haven't seen, what you might not have been taught in the MPH or related courses, and then sort of focus on that. It's hard to say, I think for the question, if there's a particular order of topics that you should tackle is some of the first slides that I put in there is that the OM examination is really, it's 60% plus clinical. It's really a clinically focused exam. And so if you wanted to be, not so much about the order, but I guess if you wanted to put weight on something there, you would put weight on clinical occupational medicine and then on the bigger aspects of clinical OcMed, which would be musculoskeletal disorders, pulmonary, infectious disease, neurotoxicity, know enough about some of the other things that tend to show along the way, like hearing loss and the like. But if you don't know clinical, you're gonna have a hard time with the exam. If you do know clinical, you'll have an easier time and then you have to more or less just kind of brush up on some of the other areas, the administrative aspects of the like. I tend to like to focus as sort of the written materials, it's June, I think it's easier to start learning and it sort of embeds better if you're able to study in July and August and not start in late September and try and catch up with it there. So two hours, two to three hours a week or something like that early in June and July are gonna pay off dividends because you'll sort of retain the stuff and understand what you go back for there. So that's kind of some guidance for organizations. Some of it is dependent on what you've already learned. Some of it is dependent on what you're studying. Styles is, and a lot of it is dependent on what happens between now and September, October because for those of you taking the boards for the first time, you're also probably lighting out and getting a job, potentially moving and also probably in these days right now, a lot more is going on with all of that and nothing is very simple. So that's kind of my brief guide to that there. I'm not totally sure if that answers things but we'll try and help along the way and sort of listen to the lectures, use the lectures, use LADU as a guidance in particular for the things that you're not understanding as well. And I think the pass rate is high amongst people with residency trained occupational physicians, pass rate is pretty high. If you're recertifying, the pass rate is very, very high. I'm not sure I know of anybody who failed it. So with that last question, anybody last? Otherwise I'm gonna be back here tomorrow doing the same thing. And you can think of questions in the meantime there. So if there's a last question, I'll answer it. Otherwise we'll knock off for the evening and wish everybody a good evening. Everyone's okay? Okay, we've got a chat light coming on here. Thank you. Okay, thank you everyone. And we'll see you again tomorrow night then if there are no further questions there. Let's see, one more. Okay, great. Thank you, Dr. Meyer. Thank you all, all right. Thank you, Bernice. All right. Okay, I'm gonna sign off. Take care, bye-bye.

clinical occupational medicine

occupational diseases

management

treatment

American Board of Preventive Medicine

guidelines

exam focus areas

questions

discussion

study preparation

weakness areas