Computer generated transcript

Warning!
The following transcript was generated automatically from the content and has not been checked or corrected manually.

um, okay. Uh, okay. So it is seven o'clock. We'll get started. Thanks, everyone, for joining this evening. Um, so my name is in each. I'm an F two. And welcome to Central. See dermatology. So we'll be doing three month course on Those are different topics and dermatology, which would be relevant to many foundation year doctors. Um, in terms of becoming more familiar with dermatological presentations, um, how to kind of diagnose conditions, how to describe Lesion's and basically a guard on how to do referrals. Um, so the first lecture will cover mainly most of these. Um, so I'll just share my screen. Can everyone see my screen? I'm gonna take that as a yes. If you if you can't someone just say I can't see my screen. All right. Cool. Thanks. Okay. So we're going to a quick run through of the contents today. So the reason we've started to do this series is because a lot of our undergraduate damn cultural teaching is not that great. Um, mine was really boring. It was just some lectures on Zoom because it was covid. So when you start foundation yet, I'm just really clueless about how to do a referral. Um, how to describe Asians, and it's quite embarrassing. Um, so quick, contents and intro. So we're gonna start with a basic reminder of the skin. Um, and some of the stuff you might have forgotten from med school. So kind of function, some fun facts, and then I'll run through the gross anatomy, um, cell type structures of the skin. Then we'll run through how to take a nice, thorough history and examination with the key points and lastly, uh, some key tools and phrases to help you when describing lesions and making your referral. So to start with, the skin is the largest team in organ making up 15% of body weight. It's an extremely dynamic organ, So there's a constant turnover of epidermis and the cycle of renewal and regeneration of the epidermis roughly last around 40 to 60 days. So it means probably half the dust at home is is going to be Baghdad skin. And I like to think of the skin as a canvas of systemic disease. So it kind of beautifully reflects reflects the state of organs. So we have an example. Here is the butterfly rash and SLE And then we have the most subtle erythema and erythema nodosa um, which is inflammation in subcutaneous fat seen in cases of inflammatory bowel disease. So the skin has a multitude of functions, so first of all, it's protective. It gives us a literal mechanical barrier, protecting our internal organs from the external environment and bacteria chemicals. Um, and another aspect of protection is the UV protection. So we get that from the pigment melanin, which protects our d n A. And it's also why we turn in the light. Um, is that's increasing melanin production. Um, the skin also regulates our temperature as arterials in our dermas dilate and constrict in response to the environment and sweat production from crying glands. So when it's hot, this leads to convection, and then that takes heat energy away from our bodies. And we also have a huge network of nerve cells, so of heat, cold touch pain and neuropathy here leads typically loss of sensation in this area. So, for example, leprosy, you have inflammation to the nerve fibers and that leads to hyperesthesia in the affected areas. Um, the skin also plays a huge role in metabolic regulation. So you be light in juices, karate insights to produce vitamin D and that contributes towards calcium homeostasis. Um, the skin also has an immune function. It fights pathogens through the dendritic cells known as Langerhans cells, and that's through fatty cytosis. And last but not least, it regulates the secretion and absorption of molecules, not stay. The skin thickness varies is based on your on an anatomical location, age and sex of the patient. So the epidermis is thickest on the palms and soles, and it's thinnest on the eyelid and skin behind the ear. Um, the dermis is thickest on the back, and subcutaneous tissues are quite obviously thickest in abdomen and buttocks, which are fatty areas. Uh, mail skin is actually 20% thicker than female skin, and that's because the collagen content of mail skin reduces at a constant rate, whereas female skin is affected more later in life, especially after the menopause. And here we have a back to basics diagram of the skin, and it's makeup, so it's basic, but it's essential and working top to bottom. We've got epidemics first, which consists of five layers of cells. We've then got the German epidermal junction containing the basement membrane got. The germ is which consists of the superficial papillary and deep particular layers, and finally we have the fatty subcutaneous tissue, so to start with the epidermis. Epidermis is, as we said before the most superficial part of the skin, and it's comprised of five layers or strata and consists of epithelial tissue, which predominantly has four different cell types. So that's karate insights, melanocytes, Langerhans cells and Merkel cells, and they each have their own function. But they work synergistically to perform as an organ, so keratinocytes are the predominant cell type of epidemics, and they originate in the basil i e. The deepest layer of the epidermis, which is called the stratum bizarrely. And they produce a huge range of different keratin's, which are structural proteins in skin and hair, nails, hair, nails, hair, nails, hair and nails. Um, they successfully form the epidermal water barrier by making and creating lipids as well as producing vitamin D. As we mentioned before, Uh, so you be be likes, hits them and activates cholesterol precursors and that form of vitamin D. The next cell type to go through is melanocyte, so it's very important. So you can see where the arrow is. There's a little melanocyte sat there in the basal cell layer next to all the other keratinocytes, and the reason for this is because of the mechanism of how pigment is produced and subsequently transferred to Keratinocytes. So Milana sites are dendritic cells, and they make milana zones, which are spherical organelles containing the pigment melanin. Um, UVB light stimulates melanin secretion, which is protective against Stevie Radiation, and it kind of acts the built in sunscreen so it protects the cell nuclear from U V E N G. Stam itch. And interestingly, the difference in shade of our skin is not the number of melanocytes but the number of milana zones. So in dermatology, we use the Fitzpatrick skin fota type scale to assess someone's risk of developing skin cancer. So, as opposed to simply saying someone's a Caucasian male or Asian female. Using the scale is much more helpful. Um, and it's definitely good to have as part of your assessment of a patient to put into a referral. So here's what I made earlier. Um, so Type one has pale white skin, always. Burns does not tan, so kind of like Taylor Swift. Type two is white skin. Burns easily tans poorly, so thinking more do a leaper. Type three is light brown skin tans after initial burn. Um, type four moderate brown skin burns minimally tans easily. I would say I'm type four or type five. Dark brown skin rarely burns darkly, and type six is dark brown or black skin. Never burns. Always cans darkly, Um, and the last the last woman in type six. Don't if you know, but she's actually a model who has with tell ago, which I think is quite cool. Um, it's called Winnie Harlow. Um, and now you have all the skin cancer risks and Fitzpatrick prototype in your favorite celebrities. And so back to Milana sites. Uh, these melanosome czar then transferred to neighboring keratin sites as we mentioned before, and that's by a process called Oxytosis. So Milana sites have long process is as their dendritic cells, and these go straight into the cytoplasm of the carotid sites, which engulfs them so you can see that nicely in the diagram. Um, and that's known as pigment donation. So I've included some microscopy images here, as I think this process of protection I think it's really beautiful. So the top left image a shows a light microscope. Microscopic image of pigment lobules inside keratinocytes. Um, so they freshly undergone some fatty psychosis. And then image be is a scanning electron microscopy image capturing pigment globules on the surface of the keratinocyte. And then that image D we can see whether arrow is that the Globe Eagles getting wrapped up by the long extensions we imagined before and in the last two have just included some transmission electron microscopy images where you can see globules trapped inside the keratinocyte. So I just think it's quite cool. Um, the next type of cell will go on to our Langerhans cells, so they're mainly found in these starting Spanos. Um, and they're also dendritic cells. They are antigen presenting cells which activate T cells and help the body to recognize allergens. So it contributes towards that immunosurveillance function we discussed earlier, and they also have characteristic dendritic processes. But unlike melanocyte, they are not connected to adjacent keratinocytes. And really, interestingly, UV radiation decreases the number of Langerhans cells, which partially explains the mechanism behind using poo va and narrow band UVB light treatment for psoriasis and eczema and the next type of cell. We'll talk about our Merkel cells, and they contribute towards the function of McCann, a reception. So they're specialized nerve endings for sensation and of note. They can lead to a rare aggressive skin cancer known as Merkel cell carcinoma, So we'll go back to the epidermis. So the way the epidermis works is that there's a constant migration of keratin sites from the bottom basal layer all the way to the top and all the cells we just talked about, all positioned at different areas, different readings through these layers. So we've got columnar regenerative cells, which are formed at the bottom, and they divide. And as they mature, they move up in the world and they lose their nuclei and all their other organelles, and they flatten out. And that process is called characterization, and eventually this forms a top layer of stat flattened, hardened cells. Um, which form that barrier function we talked about so you can see that the top and I mentioned earlier. This whole process takes roughly 40 to 60 days, and it's kind of like self renewing X radiation, which is nice to think about in the context of, you know, our own skin care routine so you won't have overnight results with your new retinal cream, you're gonna have to give it a month or so to kind of see the results, so we'll start off with the Strattera Society. So that's the deepest layer of the epidemics, and it's located just above the dermis. Um, it's the first place keratinocyte are made, and it's actually composed of around 10% of stem cells. So the cells from here divide, flatten, mature and move up, and as they move up, they go towards the surface of the skin, and Keratin's five and 14 are expressed here. And that's, uh, important when we think about diseases. So in certain people, characters 5 14 can be mutated and that kind of leads that leads to epidermal OSIs Pelosis simplex. So it's an autoimmune disorder. Autoimmune. It's an autosomal dominant disease, um, so mutations in four and 15 lead to the skin being more vulnerable to blistering, and it kind of highlights the intricate layers and structure of the and the content of the skin and has such an impact on the function of our skin and what we see and the cause, missus. So as you can see, it's very painful, and the scarring can even lead to reduced joint ability. You can see up in the top in that photo, and with very severe cases which present from birth, you can get widespread blistering, which even affect the GI tract. And that obviously has an impact on feeding. For these infants, Um, treatment is mainly on caring for blisters and preventing new ones. Um, so next up is the stratum spinous, um, so that's also known as the prickle cell layer or the scar muscle layer so we can look at each layer of the epidermis as kind of stages of differentiation. So it's named the Prickle cell layer or starting Spinoza because it consists of intercellular bridges called desmosome, and it gives it a kind of spiny appearance. Um, and the desmosome aid the keratin sites and kind of sticking together in this new layer as they become flattened and they move up. And thickening of this layer is known as a canthus ISS and Keratin's one and 10 are expressed in this layer, and when they're mutated, that leads to something called epidermal otic ichthyosis iss. So again, it's an autosomal dominant condition. Um, and about half of cases are GT new mutations in keratin one and temp, So they're not always inherited. Um, and it becomes apparent of birth where the reddening scaling. So they're blistering, as you can see in the image. Awful and hyper keratosis develops within months, and it worsens over time. So just to highlight the absolute breakdown of some of the core functions of the skin we discussed earlier can lead to such a devastating picture. So even basic nutrition when it comes to impact on mucosal membranes is affected. Uh, the next layer is the start. Um, granulation. So on H and E staining this layer is the darkest, uh, the dark purple layer due to dense Kurata, highline Granules and lamella Granules, which contain keratin precursors that eventually aggregate crosslink and become bundles. So the lamella Granules contain like a lipids that gets secreted to the surface of cells, and it kind of functions as a glue, and it keeps those cells stuck together and forms this corn ified cell envelope so thickened it thickens in scratching and rubbing. For example, in lichen planus you get hypo Granulosus and this layer Next, we're gonna go into the stratum lucidum. So there's not much to say here. So it's only found on the palms and soles, and you can see as this thin, transparent layer here so you won't see it in all images unless it's of the palm or the soul. Um, so the terminal layer of differentiation. The last one is called the stratum corneum, and it's made up of interlocking layers of dead stratum. Corneum cells basically anucleate squamous cells, and this is the layer that varies the most in thickness. We were talking before about the thickness of the skin. This is the layer, um, so we describe the slayer as a brick and mortar structure with the bricks representing the anucleate keratinous sites, which are all embedded within all of these intercellular lipids and the corneum and granny loosen. These layers are not on mucosa, so thickening of this layer is known as HIPAA keratosis. Increased thickness of the stratum corneum can be due to loads of different stuff so it can be due to exogenous or endogenous processes, and it's related to the increased production of kerosene in the outer portion of the skin layer. And in the majority of cases in clinical practice, it's mostly due to chronic physical or chemical damage, like friction or the use of aggressive soaps. So with asthma, you don't have a strong lipid barrier as much, and the lack of moisture dries out. Skin makes it damage, and it's easily inflamed. Okay, next, we're gonna go on to the D. E. J. So the dermis is just below the epidermis and the to connect at something called the Dermo epidermal function. And it's the interface between the stratum nasally and the dermis. So the D. J is important because it provides a structural support and allows the mediation of signals allowing for epidermal renewal and regeneration. And it has these wreaked bridges and their downward projections of the epidermis into the dermis, which you can see really clearly on the diagram. Um, and it kind of reinforces how the layers are locked together nicely and flattening. Flattening of this D e. J actually enhances wrinkling and aging fy. I, um, say the dermis consists of two layers, the superficial papillary layer and the deeper, particularly, um, consists of egg nexus. So sweat glands, hair, hair follicles. This is where all of it's at, and it also has fibroblasts. So, um, with collagen, elastic fibers and glycosaminoglycans so fibroblast produce collagenous and elastic fibers. It's mainly type one in the dermis, and collagen and elastic fibers provide the support and elasticity for a matrix, which underpins healthy skin and is a key determinant to the preservation of skin firmness and elasticity naturally by the names. So from early adulthood, fibroblasts actually become less active and collagen production declines by about 1% a year. So for any of you who do take college and supplements to supplement drinks, those containing hydrolyzed collagen peptides apparently can improve skin elasticity, hydration and signs of fine lines and wrinkles. But I'm not too sure about the data on that. Actually, it's a hypothesis, but no one said not to take it. So, um, and talking about stuff that's more backed up by data retinoids and vitamin A products they actually up regulate the production of collagen. And also UV radiation has an impact as well as hormonal changes. So the decreased production of collagen after menopause, um, is because, well, it reflects estrogens and progesterones decreasing as well. Um, so steroids also down regulate collagen production, which is why atrophy is a side effect. Um, and another product of fiber blast metabolic function is the production of glycosaminoglycans and one of the big molecules to talk about here is hyaluronic acid, which the humectant. So it absorbs moisture from its surroundings. And with that, it creates plumpness and volume, which we associate with youthful skin. So talk a topical. You can use it as a medicine, um, as a moisturizer, basically. So it goes on top of your head keratinocyte on your Straaten for some temporary plumpness, if any of use the humble ordering products, That's what's doing. Um, but aha is also crucially used in dermal fillers. So by doing that, I get straight to the dermis because it draws in water to replace lost volume, and it kind of enhances the filling effect so you can see that and the lip fillers there. Okay, so going back to the papillary dermis. So this is the thin layer composed of loose a connective tissue, um, and a thin layer of collagen, and it contains the supper pillory plexus. It has arterials, capillaries, venue ALS, nerves and it's it contributes towards temperature regulation and supplying the circulatory supply for the epidemics so very important. And the thicker collagen fires fiber's really contribute because it also supports the other components of the skin, like the hair follicles, sweat glands, Salvation scan. So you need you really need that support in this layer. Okay, so that was a quick whistlestop tour, and we're finally going to go on to history taking and examination. So first of all, start with focusing on the presenting lesion and the presenting complaint. So start asking general questions to gain information. When the rash started where it started, the site the duration. And, as with any presentation, if they're able to let the patient describe the lesion to you, consequently, you want to ask about associated symptoms. So particularly for dermatology, you need to ask about kind of associated pain, itch bleeding or any pass associated with the lesion, Um, and always ask about triggers and alleviate ear's. So it's important to ask whether anything makes things better or worse. So, for example, stress trigger flare of psoriasis, the very basic example, but very important to ask or certain medications can flare. Carrier so incense, and it's very much worth asking if they've ever had any injury to the area as well, because of injury responses. So the covid a phenomenon describes the appearance of new skin lesions, all the pre existing disease in areas where there was before. Healthy skip. So it's associated with plaques arises for till ago with kind of patches of hyperpigmentation. Um, on the other hand, pathology is can be confused with covid, a phenomenon. Sometimes the pathology is a more generalized response to trauma, with the formation of popsicles and posture. So it's not because of a preexisting disease. Um, and pyoderma Gangrenosum also presents very also presents like this. So there's a rapidly enlarging, very painful ulcer associated with IBD, and that shows pathology so going back to the history taking. So the next step is looking at occupational and social history. So smoking, alcohol, drugs, substance abuse, all of which can flare and trigger certain conditions and definitely ask about medications. So allergies pets as well, um, very crucial with dermatology and next up would be traveling in recent contacts to ask about any travel definitely relevant for infestations or tropical skin infections, and also make sure you ask about covid 19 vaccination history so vaccinations can flare and even trigger both existing and new rashes. So vaccinate vaccination dates and history are very important, especially in the current climate. And you definitely want to ask about past medical history. So, for example, some dental conditions are associated with systemic disease. And also you have the atopic triad. So atopic dermatitis, allergic rhinitis, asthma. And then finally, you want to do a systems review. So ask about systemic symptoms fever, weight loss, um, any symptoms in other sites, Kind of secondary dermatological sites. So mucosal membranes, joints, scalp slash hair and nails They can all be linked. And I just wanted to touch upon speak. We spoke about drugs before we don't go into it. Um, also substance abuse. So this is a really interesting case where you can have levamisole adulterated cocaine vasculopathy. So it's basically retta form purpura, which you can see in the images, um, in the limbs. And this is this is really rare, but I just think it's really cool and highlights the importance of why you need to do a detailed drug. Alcohol is making substance abuse history. Um, for drugs, especially, go back three months, three months back. The effects can be that long. Um, and so this is actually characterized by a pathetic rash in a Rathbone pattern and has a predilection for the ears. And it is associated with anchor positivity. Very interestingly. So, um, also important to ask about the psychological aspect. So skin disease has a huge negative emotional impact on patients', and the severity of the disease doesn't really matter, so it doesn't correlate with how the patient feels. Um, someone with a mild form of eczema can end up having severe depressive disorder or be at risk of suicide. On the other hand, you might find someone within something as awful as pyoderma Gangrenosum, which we discussed earlier, would just have some mild anxiety over it. So it just never doesn't correlate all the time. So you have to always assess how it can affect your patient, the self esteem, mood, body image and confidence. And there's a parliamentary report very recently discussed and published this year. I think it was January, and it's pushing for more funding and pathways, um, for kind of support in clinics and psychedelic logic clinics as It's very rare at the moment. I think there's only six psychedelic logic clinics in the country, so skin cancer specific. So when you're examining a lesion that might be cancerous, the specific questions that you need to keep in mind So you need to look at the initial appearance and evolution of the lesion, which is similar to what we did before with any skin condition. Um, and it's definitely still worth asking about any medications that can cause a meaner suppression. Definitely ask about previous and current treatments and whether they were effective or not and whether this is a recurrent and you need to get some relevant information on previous personal history and family history of skin cancer, any previous history of sunburn or the use of sun tanning machines, as well as any long periods of sun exposure or living in a tropical climate, you need to ask about problems with nail scalp, hair or joints, like we said before and as I already mentioned previous history of this disease. So we discussed earlier the formal tool used and dermatology for categorizing different skin fota types, and it's called the Fitzpatrick Scale, so richly pigmented skin can also be affected by cancer. Um, for example, a cool areas, so don't always dismiss someone with darker skin. They also may have cancer, so it's not always just type one type two. Type three. We're gonna move on to the down political examination, so there's four principles to a derm exam. So Number one is to inspect the lesion number. Tears describe it, which we will touch upon after. Don't worry. Number three is PAL patient, and number four is a quick, systemic track. So start off with the general inspection of the patient. Note the Fitzpatrick skin prototype. Look at the number and the location of lesion, so you will need to expose your patient. The big mistake is only looking at the one area which the patient is presented with. When you keep in mind that dermatology is not just skin, you have to look at systemic disease. You need to be exposing your patient and seeing where the other lesions are, so don't fall into the trap of just looking at one lesion. Um, look at the distribution and the configuration of lesions on the body configuration refers to the shape or outline of skin lesions. If you didn't know, um and then how to describe a individual lesion. So I like to use scam. So f is the size, so use the widest diameter S is also for shape. C is for color. A is for any associated secondary change and we'll come onto that. M is for morphology or the margins. And furthermore, you need to be assessing for pigmented lesion's. And when I say that, I mean that referred to cancerous lesions say pigment occasions. I think we all know this from med school. It's a B C D approach. So the presence of any of these increases the likelihood that this diagnosis is malignant melanoma and you need to investigate further. So a slight asymmetry B is for borders. Irregular C is for colors. Got different shades, so that's really awful in the image there, um d is for diameter. The lesion is larger than six millimeters alarm bells going off, and it is for evolution. If it's continuously changing, it's worrying. Okay, so we're going to move on to describing the lesion. So big topic, but really important. And it's not too bad once you get through some of the basics, which I'll go through today. So there's two types of skin lesions. There's primary and secondary, so primal Asians are unmodified lesion's, so they're either their from birth or they're directly from a disease. For example, um, directly from an infection, an allergic reaction, your environment or you can have a birthmark like a hemangioma. These are all primary lesion's secondary skin lesions are evolved from Primary Lesion's when they've gone through, say, trauma, further infection or same medication. So an example of that would be crusting from scratching your eczema and the exploration from that. Or if you have an infective allergic wheel, or like an ification of the epidermis from all the scratching. These are all secondary skin lesions. So how to communicate your findings in your referral? We're going to get to some describing Lesion's so communicating morphology for primary lesion. So look at the structure of the lesion, so flat lesions are either macula's or patches. If they're macule, they're tiny. They're less than one centimeter. If they're patches, they're over a centimeter, and that's all solid raised Lesion's. These are not fluid pills. If they're Papular is, they're tiny. They're less than 0.5 centimeters. And if they're plaques but over 0.5 centimeters, for example, in psoriasis and the populace, I put an example of milion here. Nah, jewels are having more rounded and deeper component. So Molluscum contagion Asian and it's pearly nodules is a good example, And a morbilliform rash is a mix of macular and pop pills, so we call them drug and bug rashes. Okay, so previously these were not fluid fold. They were solid but not fluid filled. These are raised but fluid filled with any tax. Those physicals, which are tiny, less than 0.5 centimeters, and bowler, which are big, so zero point over 0.5 centimeters, so an example of vehicle would be contact dermatitis of the hand. An example of below very easy bullous pemphigoid and something I find really interesting is special skin test for bolstering lesion. So it's called a Nicole Nicole skis test. Um, so it's normal on skin around the bowler, but it's Nicole ski positive when natural pressure on unlisted skin cause the shearing of the epidermis. So, for example, if you're rubbing in a razor on the skin, that's Nicole ski sign positive. So It's also positive in Steven Johnson syndrome and pemphigus vulgaris, but it's negative in bullous pemphigoid because this is a much deeper skin process. Okay, so, uh, the lesion's to talk about our postural so postural czar Small past containing lesion similar to physicals. But they've got passing them, um, for wrong calls from staphylococcal infection around or within a hair follicle and carb uncles are just saying multiple for uncles. It's just a fancy way of saying that. And wheels are transient raised lesions due to dermal edema. Um, so you can see the examples. Here we have something called folliculitis keloid artists, and that's an unusual form of folliculitis. So it's information of the hair follicle unit and further to that alopecia alongside that, and that kind of affects the nape of the neck result, as you can see there and then we just have a nice example of wheels on the bottom. Okay, so second relieve in exploration is the loss of epidemics following trauma. Um, so scratching lesions from eczema would be an example. A fissure is an epidermal crack, often due to dryness and its typically in thick, dry skin to you. I'm sure everyone's had fissures in the hands heels, corner of the mouth and like unification is a term to refer to the well defined rough inning of skin with accentuated skin lines so you can see that on chronic dermatitis. Scaling refers to flakes of that top layer of skin, the stratum corneum so plaques and psoriasis thin plaque in pityriasis versicolor. A nice description that would be scaling crossed is essentially a rough service surface, and it consists of dried up content so dried up said, um, sebum blood cells. Puss. Um, for example, you can get it from a burst vista, Um, and you can see a nice example of honey colored blisters in for tiger you can describe those crust Ulcers are described as excavation, which reach the epidemics and the dermis so they heal with scarring because damage doesn't have renewal and regeneration. So you're going to have scarring them. Um, and in terms of scars, scarring is basically new Farber's tissue after healing, um, atrophic scars like thinning hypertrophic scars are hyper proliferation within the wind boundary and the difference between kilo dull and hypertrophic scars, uh, the keloid or goes beyond the wound boundary. So keloid scars firm Smooth, Hard Um, and it can arise soon after an injury or develop months later. And they can be really comfortable, uncomfortable in a tree and extend way beyond the original wound. So the next step is PAL patient, So we need to palpate in order to assess surface and consistency of a lesion. So first we'll look at the surface or texture of the lesion, or feel the surface or texture of the lesion. Is it rough? Is it smooth? Is it an elevated or is it depressed lesion? So, for example, an elevated lesion would be a karate camp coma. Arctic area, and it's wheels depressed lesion lesion would be hypertrophic scarring, acne. As we mentioned before, you can see a nice example of hypertrophic scarring in acne. We felt that we felt depressed lesion. We'd feel a depressed lesion and then look at the consistency. So is it hard or is it soft? I e. Is that fluid inside? Is there solid inside, for example, soft pass versus hard keratin inside the lesion. So, Amelia, you've got lots of tiny, very small thoughts containing keratin. Um, whereas a cutaneous horn is completely elevated solid with hard Carrington, um, and then look at whether that structure is mobile. So is it on its own? Is it moving, or is it linked to other local structures? Um, look at whether it's tender or is there a kind of temperature or palate to your lesion? Um, that'll help you kind of think about whether it's effective or inflammation. So lastly, dermatology includes not just the skin. As I mentioned many times, uh, it's really important to check other areas. So hands, mouth, scalp, nails, and not just those, but to completely expose a patient and check other areas. So genitals, abdomen back everything, um, and also general examination, um, of the other systems, if they're suspected systemic disease. So I've mentioned SLE, IBD, thyroid and psoriasis quite a few times. Um, and finally, I just wanted to go through how to describe a lesion and kind of formulate and kind of get it set in your brain a bit more easily because I know we've gone through loads of different stuff. Those are different words. It's going to be hard to get your head around how to kind of put those together when you're describing lesion making a referral, So I like to use a pneumonic called less T calves. So l is for location. So you see a lesion. First things first. Where is it? Is it on the air? Head abdomen? Is it localized somewhere? Is it in a sun exposed areas? So it's on the face. Scalp air. Is it symmetrical? Um, dermatomal all different ways to describe the location. So you're just focusing on the location. For example, we have a unilateral dermatomal heard Perthes officer at the top, um, and then eat erythema. So redness in and around the lesion's I feel like most lesions have some erythema. Um, you're probably going to comment on that anyway, um, but really important to still make a comment on, um and then f for surface. So think about the surface of the lesion. So you've already done your pal patient. So you know, you know how your lesions feel, So it's smooth, rough crusted, scaly. Then we move on to t. So think about the type of the lesion. So is it primary or secondary? And we already know the difference is, uh, the think of the color. Is it pigmented? Is it hyperpigmented like vitiligo and then look at the arrangement, a k a. The configuration. So how are the lesion's arranged in relation to each other? Um, and so they can be group, so you can have generalized, uh, it could be unilateral in a ring shaped Aniela and then think of be for borders. So the demarcation of lesion's is important. So, for example, um, cellulitis would be well demarcated. So you'll say you'll describe that's a well demarcated lesion, um, and then s for special sites. So I've said the snails, scout pans, genitalia, mucous member into secondary dermatology. Um, And when communicating distribution, a couple good terms to you so generalized would be all over the body. Uh, widespread would be completely extensive. Localized would be restricted to one area of the skin, uh, Flexeril in the body falls and neck property, and to keep a faucet, cubital fossa, groin and then extensile, uh, be knees elbow insurance. So you can see you have a nice extensile, a plaque of psoriasis in the extensor area. Um, and then also pressure areas is quite good to look at, So sacrum buttocks, ankles, heels. I've mentioned before Dermatobia all regions and also photo sensitive areas. So face here, here, here, here he lyses and the scalp. So how to communicate configurations so discreet would mean individual separated lesion's, uh, complement would mean lesions emerging together. Linear is very self explanatory. Um, target lesions. So these are typically always erythema multiple. Um, they're kind of concentric rings you can see on that person's hands there and then annular or disco illusions are classically kind of tin eared corporate. You can see a really, really nice example that OK, communicating color. So we've already mentioned erythema. I feel like loads of solutions have an erythematous base. Um, so erythema is redness which blanches on pressure Per pere is the red or purple color which does not blanche on pressure. So if you're ever wondering how to differentiate, you've already got that. They're hyperpigmentation is area areas of paler skin. Hyperpigmentation is very self explanatory. Areas of darker skin and deep pigmentation is white skin. Due to the complete absence of melatonin militant melanin. Sorry. Melanin. Melanin. Okay, um and yeah, Thank you so much for listening to the talk. I hope it was useful. Um, and I just got a QR code there for feedback if you guys wouldn't mind filling it out. And we have quite a few talks coming up. So we're going to have a 12 week lecture series. So next week, we're doing inflammatory diseases and we have a whole line up for the next 12 weeks. If you check on Facebook, you can see all the different talks we're going to be doing every week. Thanks so much, guys. I hope it was useful. And yeah, I already mentioned the feedback form. Oops. I'll just leave it here for a bit. I think you should be emailed it often, but I'm just going to keep the QR code open. Um, if I don't have the link on me right now or I can email you the link actually Sophie Friendly. Yeah, I don't worry too much. You should be emailed the feedback link after as well, anyway. But I just think a QR code is much easier. I find it easier. Okay, Cause like I said, if you look out for the Facebook event, page is for our next talks. Thanks so much for joining. I hope it was useful. Um, it's kind of stuff which I think is interesting and also relevant. Um, so yeah, I'll see you guys next week