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You are here: Home / Podcasts / 154 Derm Patterns That Give You Easy Points – Hair, Nails & Rashes

154 Derm Patterns That Give You Easy Points – Hair, Nails & Rashes

Get 26 Dermatology questions straight from The Final Step.

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Alopecia

  • Hair loss disorder with multiple etiologies

Clinical Presentation

Alopecia areata

  • Sudden onset
  • Patchy, well-circumscribed, non-scarring hair loss
  • Smooth scalp skin
  • Exclamation-point hairs (short broken hairs that taper proximally)
  • Associated with autoimmune disease (thyroid disease, vitiligo)
  • Nail pitting may be present

Androgenetic alopecia

  • Gradual, progressive thinning
  • Men: receding hairline, vertex thinning
  • Women: diffuse crown thinning with preserved frontal hairline
  • Strong family history

Telogen effluvium

  • Diffuse hair shedding
  • Occurs 2–3 months after physiologic stress
    • Illness
    • Surgery
    • Pregnancy
    • Emotional stress
  • Positive hair-pull test
  • Scalp appears normal

Tinea capitis

  • Patchy hair loss with scale
  • Broken hairs (“black dots”)
  • Common in children
  • Posterior cervical lymphadenopathy

Scarring alopecia

  • Permanent hair loss
  • Loss of follicular openings
  • Inflammatory or autoimmune destruction

Diagnostics

  • Clinical diagnosis
  • KOH or fungal culture if scale present
  • Consider TSH if autoimmune disease suspected
  • Preserved follicles = non-scarring
  • Absent follicles = scarring

Treatment

Alopecia areata

  • Intralesional corticosteroids (first-line)
  • Topical steroids as alternative

Androgenetic alopecia

  • Minoxidil
  • Finasteride (men)
  • Spironolactone (women)

Telogen effluvium

  • Reassurance
  • Remove underlying stressor

Tinea capitis

  • Oral antifungals (terbinafine or griseofulvin)
  • Topicals alone ineffective

Exam Keys

  • Patchy, smooth hair loss → alopecia areata
  • Diffuse shedding after stress → telogen effluvium
  • Gradual thinning over years → androgenetic alopecia
  • Child + scale + broken hairs → tinea capitis
  • Loss of follicular openings = scarring and permanent

Onychomycosis

  • Fungal infection of the nail (dermatophytes most common)
  • Toenails affected more often than fingernails

Risk Factors

  • Older age
  • Diabetes
  • Peripheral vascular disease
  • Immunosuppression
  • Tinea pedis
  • Nail trauma
  • Occlusive footwear

Clinical Presentation

  • Thickened, brittle nails
  • Yellow-brown discoloration
  • Subungual debris
  • Onycholysis
  • Often asymptomatic
  • Thickened, yellow, crumbly toenails in the stem

Diagnostics

  • KOH prep
  • Fungal culture
  • Nail clipping with PAS stain

Treatment

  • First-line: oral terbinafine
  • Alternatives: itraconazole, fluconazole
  • Topical agents (ciclopirox, efinaconazole) for mild disease only
  • Fingernails: ~6 weeks
  • Toenails: ~12 weeks
  • Monitor LFTs with systemic therapy

Exam Keys

  • Thickened yellow toenails → onychomycosis
  • Oral therapy required
  • Terbinafine = first-line
  • Topicals usually fail

Paronychia

  • Infection of the lateral or proximal nail fold
  • Acute or chronic

Risk Factors

  • Nail biting
  • Manicures or artificial nails
  • Frequent wet work
  • Diabetes
  • Immunosuppression

Clinical Presentation

  • Acute: rapid onset pain, erythema, swelling, possible purulence
  • Chronic: swelling, erythema, nail dystrophy >6 weeks
  • Usually Staphylococcus aureus (acute)
  • Tender swelling along nail margin in the stem

Diagnostics

  • Clinical diagnosis

Treatment

  • Warm soaks
  • Incision and drainage if abscess present
  • Oral antibiotics covering Staph
  • Chronic: avoid moisture, topical steroids ± antifungals

Exam Keys

  • Nail fold infection → paronychia
  • Acute = bacterial
  • Chronic = inflammatory
  • Abscess → drainage

Felon

  • Deep infection of the fingertip pulp
  • Closed-space infection with risk of ischemia

Risk Factors

  • Puncture wounds
  • Splinters
  • Untreated paronychia
  • Diabetes
  • Immunosuppression

Clinical Presentation

  • Severe throbbing pain
  • Tense swelling of fingertip pad
  • Pain out of proportion to exam

Diagnostics

  • Clinical diagnosis
  • X-ray if concern for foreign body or osteomyelitis

Treatment

  • Urgent incision and drainage
  • Oral antibiotics covering Staph and Strep

Exam Keys

  • Pulp space infection → felon
  • Severe throbbing pain = key clue
  • Requires drainage

Pigment Disorders

Melasma

  • Acquired hyperpigmentation of sun-exposed skin

Risk Factors

  • Pregnancy
  • Oral contraceptives
  • Estrogen therapy
  • Sun exposure

Clinical Presentation

  • Symmetric brown or gray-brown facial patches
  • Cheeks, forehead, upper lip
  • No scale or inflammation

Diagnostics

  • Clinical diagnosis

Treatment

  • Sun protection
  • Hydroquinone (first-line)
  • Retinoids or azelaic acid

Exam Keys

  • Symmetric facial hyperpigmentation → melasma
  • Pregnancy/OCP association
  • Sun worsens it

Vitiligo

  • Loss of melanocytes causing depigmented skin

Risk Factors

  • Autoimmune disease
  • Family history

Clinical Presentation

  • Well-demarcated white patches
  • Face, hands, periorificial areas
  • May have white hair (poliosis)

Diagnostics

  • Clinical diagnosis
  • Wood’s lamp accentuates lesions

Treatment

  • Topical corticosteroids
  • Topical calcineurin inhibitors for face/intertriginous areas
  • Phototherapy for extensive disease

Exam Keys

  • Depigmented patches → vitiligo
  • Autoimmune associations common

Chronic Inflammatory Derm

Acanthosis Nigricans

  • Velvety hyperpigmented plaques
  • Marker of insulin resistance

Risk Factors

  • Insulin resistance
  • Obesity
  • Type 2 diabetes
  • PCOS
  • Malignancy (rare)
  • Higher prevalence in African American, Hispanic, Native American patients

Clinical Presentation

  • Dark, velvety plaques
  • Posterior neck, axillae
  • Abrupt onset raises concern for malignancy

Diagnostics

  • Clinical diagnosis
  • Evaluate for insulin resistance

Treatment

  • Weight loss
  • Improve glycemic control

Exam Keys

  • Velvety plaques on neck/axillae → acanthosis nigricans
  • Think insulin resistance
  • Sudden onset → malignancy workup

Stasis Dermatitis

  • Chronic inflammatory dermatitis from venous insufficiency

Risk Factors

  • Chronic venous insufficiency
  • Varicose veins
  • Prior DVT
  • Obesity
  • Prolonged standing

Clinical Presentation

  • Erythema, scaling, pruritus
  • Brown discoloration (hemosiderin)
  • Medial ankles and lower legs
  • Chronic edema

Diagnostics

  • Clinical diagnosis

Treatment

  • Compression stockings
  • Leg elevation
  • Topical corticosteroids

Exam Keys

  • Lower leg dermatitis + edema → stasis dermatitis
  • Compression = first-line
  • Not infectious
Full Transcript (click to expand)

Hello and welcome to the Physician Assistant Exam Review Podcast. This is episode 154 and we’re going to be covering hair, nails, and a couple other things. My name is Brian Wallace. I’m the host and creator here at Physician Assistant Exam Review and I am thrilled to be here with you today because we are going to be covering dermatology, not just a few we’re going to be covering dermatology, but that honestly dermatology is not my favorite thing even close. But more importantly, we’re not just covering the medical facts here. We cover how to think about it, how to study it, how to organize your thinking, and how to perform on high stakes exams. That’s the whole point.

I’m a little charged up because we had our first meeting of the February cohort of 33 Days to Pass the PANCE last night, had some 40, 50 students on the call and just got some great feedback from them, some great insights, getting people kicked off, getting people started. It’s so much fun to get to work with students in that capacity and to see them making progress every single day. Our motto here within the podcast, within our community, within the 33 Days program is to think different, see that you work differently, so that you score differently. So many people, I was just saying today, I see on Reddit and other places, people say, you know, I’m struggling. I’m not doing well. And I’ve tried everything there is, and it’s still not changing anything. And it’s one of my, it’s so concerning because it lacks so much imagination to say, I’ve done everything there is.

It just means you’ve done everything you can think of. You’ve done everything you can, you’ve, someone else has told you. You haven’t done everything there is, right? That’s kind of a bold statement to make. And what we do here is try to show you some of those different pieces, some of those different places you could be doing work. And we do that by breaking down the medical content so you can recognize it on exams and organize it while you’re studying and avoid some of those common thinking traps, some of those common mistakes. So if you’re working really hard and you can’t figure out what the problem is, this podcast is for you.

This is the place to start. This is the place where we go through all of that material and we do it in a way that hopefully moves the needle for you. This week, we’re going to start with our priming questions and jump right into the, to the material. We always do five priming questions at the beginning of every show. That way we can sort of anchor our thoughts to where we’re going, what we’re talking about, where we’re moving. Today, we’re going to be doing hair and nails first, followed by pigment disorders, followed by some like chronic inflammatory and systemic issues that show up as dermatology questions. So for our priming questions, number one, a pregnant woman develops symmetric hyperpigmentation on the cheeks and upper lip.

What’s the most likely diagnosis? A pregnant woman develops symmetric hyperpigmentation on the cheeks and upper lip. What is the diagnosis? Patchy smooth areas of hair loss appear suddenly on the scalp. What’s the most likely diagnosis? What’s the most likely diagnosis? Diffuse hair shedding begins several months after an illness, severe illness.

What’s the diagnosis? Thickened yellow brittle nails, toenails, have not improved with topical therapy. What’s the next move? What’s the next step? Itchy erythematous scaling skin with chronic swelling is noted around the medial ankles. What’s the most likely diagnosis? What’s the most likely diagnosis?

All right. We’re going to jump in and get started, and that should give you an overview and something to anchor your thoughts to as we move through this process. Alopecia is going to be first. This is a partial or complete hair loss. This can be scarring. I’m sorry, non-scarring, which is reversible, or scarring, which is permanent.

Now, there’s a couple of different kinds, and so we’re going to go through them. I’m going to mispronounce all of them, so it’ll give you something to laugh about as we go along. Risk factors. Autoimmune disease is a risk factor. Thyroid issues certainly can cause a problem here. Physiological stressors. So at two to three months before an event, we’ll talk about that in a second.

Illnesses, surgery, pregnancy, major stress, weight loss, all these things can be risk factors. Family history and androgen sensitivity. Childhood exposure risk for fungal infections. We’ll get to all that in a second, but just you have a jumping off point. Clinical presentation. Alopecia areata. Sudden patchy well-circumscribed smooth areas of hair loss.

This is non-scarring. This you get the exclamation point hairs, which took me a minute to understand. These are short, broken hairs that taper down at the base. Definitely pull up an image there. I think it’ll be helpful. Androgenetic alopecia. This is gradual, progressive thinning.

Usually in men, receding hairline at the vertex. Women have a diffuse crown thinning frontal hairline often preserved. It absolutely happens in women. But I’d like to think if you’re going to get a PANCE question on it, it’s going to be about men. Telogen effluvium? I think. You maybe check the notes on the website to be confident there.

Diffuse shedding. Often noticed in the shower or the brush. And this starts two to three months after a stressor. So we talked about risk factors. You want to talk about psychological stress. Weight loss. Those kind of things can trigger this.

Tinea capitis is. I don’t know if it’s necessarily considered alopecia, but I include it here because we want to get test questions right. That’s our goal here, right? So this mimics hair loss. This gets patchy hair loss with scales and broken hairs. This often happens in kids. And the question stem, when we talk about alopecia, is it likely going to be patchy smooth hair loss or diffuse shedding after an illness or pregnancy or gradual pattern thinning with family history?

Those are going to clue you into the different types. For diagnosis. Well, again, what do you think? Not again, but what do you think here? What’s going to be our diagnosis? How are we going to do this? What labs are we going to do?

Are we going to do blood work? Well, this is going to be a clinical diagnosis mostly, right? If you see scales or broken hairs, what is that going to make you think? Hopefully it makes you think fungal issues. So like KOH. So you’re going to do a KOH prep for fungals. I just said that really terribly.

You’re going to do a KOH prep looking for a fungal infection, tinea capitis. If there’s some indication that there’s an autoimmune issue, you’re going to maybe consider TSH or other diseases. A treatment for alopecia areata. This will be intralesional corticosteroids are the first line topical steroids as an alternative. Androgenic alopecia, something like minoxidil. Telogen effluvium, reassurance and removal or resolving of triggers. So basically they get rid of that stressor and they should do better.

But you want to reassure them that it will be okay and it will come back. Tinea capitis, we’re going to do oral antifungals. Topicals are not going to get it done here. So if you have patchy, smooth, non-scarring hair loss, you’re thinking alopecia areata. If you have diffuse shedding of hair after some sort of very stressful event, telogen effluvium. If you have gradual pattern thinning and family history, that’s the one that we’re most commonly used to. Androgenetic alopecia.

And if you have a child who’s losing hair, the first thing you should be thinking is tinea capitis. Then throw in if they’ve got scales or broken hairs. We’re going to do oral antifungals there. Onychomycosis is next. This is a fungal infection of the nails. Usually the toenails, more than the fingernails, has to do with blood supply. I think that was what it was.

Risk factors. Older age. Diabetes. Peripheral vascular disease. Yeah, sorry. That reconfirms my thoughts that it has a lot to do with the avascular nature of nails and how far, what the vasculature is down by your feet versus at your hands. Diabetes.

Peripheral vascular disease. All those things are going to increase the risk because it’s going to decrease your blood supply. Immunosuppression. Tinea pedis. Nail trauma. Occlusive footwear. Clinical presentation.

If you haven’t seen this, it’s pretty obvious once you see it. Thick and brown. Thick and brittle nails. Yellow brown. With a yellow brown discoloration. I used to work for an orthopedic foot and ankle surgeon. And we’d see a lot of this.

Let’s just say we’d get to the OR and have to. Do some surgery before our surgery. Subungual debris can be a problem. So if someone has debris under their nail and it lives there, that can be an issue here. You can get some nail plate separation. Usually this is asymptomatic, but it looks gross. But it doesn’t really bother people.

The question stem here is going to be some kind of a thickened yellow crumbly toenail. Often in a patient with some sort of vascular issue or diabetes. Something like that. This is a clinical diagnosis, but you could do a KOH prep. Treatment is first line is going to be oral terbinafine. You can use itraconazole or fluconazole. There are topical agents, but they don’t work as well.

Like ciclopirox or efinaconazole. The problem is they just don’t work that well. But here’s the thing. The oral medications are really rough on the liver. So you have to check LFTs beforehand. That’s a major test question. And your treatment duration is long because it takes a long time to penetrate.

So fingernails is like six weeks. Toenails is like 12 weeks. One of the major keys here to me is the monitoring LFTs. Next we have paronychia. I think it’s paronychia. Definition. This is an infection of the lateral or proximal nail fold.

This is extremely painful. Can be acute or chronic. Risk factors are nail biting, manicures, artificial nails, frequent hand washing or wet work, diabetes, and immunosuppression. My youngest had this. I’m going to say, I don’t know. He was four or five years old. And it was horrible.

His finger just got really incredibly painful. A little pocket of pus formed. Just nasty right along his nail. And because he’s a nail biter. And he continues to be a nail biter some 10 years later. Which absolutely was the issue here. You have rapid onset pain, erythema, swelling at the nail fold, pain that I mentioned pain.

This may have visible purulence. The one that I saw, one my son, was absolutely like that. Most commonly, it’s staph aureus. You can get this chronically. There you have swelling, erythema, nail dystrophy, lasting greater than six weeks. It may be candida if it’s this type. So the question stem is going to describe a tender swelling and redness along the nail margin.

And often following nail biting or something like that. It’s a clinical diagnosis. Treatment is going to be mild, warm soaks. But if you have an abscess, you may need to I&D it. And get some oral antibiotics on board. Which is what we wind up doing. I actually, his sort of, I’m going to say rupture.

That’s not really the right word. But it was open. So I squeezed it and got a lot of the purulent material out of it. He was not happy with me. I spoke to a pediatrician the next day. And was told that I was a horrible human being for doing this to my son. That it’s incredibly painful.

I think they were probably right. That it was probably a mistake. And then we brought some antibiotics. And it cleared up for him in a couple of days. For the chronic kind, you’re going to avoid moisture. You can use topical steroids or perhaps antifungals if you think candida is involved.

Exam keys. This is an infection at the nail fold, right? That’s it. In the acute setting, this is usually staph. In the chronic setting, it’s usually candida.

Next, we have felon, which is a deep infection of the fingertip pulp. This is a closed space infection. So there’s a risk of ischemia and necrosis. So this is kind of like compartment syndrome in the leg. This is an infectious cause. But because it’s a closed space, if it swells, we’re looking at ischemia occurring. So risk factors here would be something following a puncture wound or a splinter, untreated paronychia, diabetes and immunosuppression, of course.

Clinical presentation is severe throbbing, tense swelling of the fingertip pad, erythema and warmth, pain out of proportion to exam. And the question stem here is just going to be intense fingertip pain and swelling following some sort of issue, some kind of injury. This is a clinical diagnosis. I guess you get an x-ray if you’re worried that there may be something in there that you could see on x-ray. This is sort of an urgent situation because it’s a closed compartment. You can get that necrosis, right? You can get ischemia.

So you have to be on this. So you’re going to do an incision and drainage, possibly. You’re going to do oral antibiotics for staph and strep. And again, you need to be really aware of this because you can cause long-lasting issues.

Okay, we’re going to move out of hair and nails and into pigment disorders. Melasma is first. This is the acquired hyperpigmentation disorder of sun-exposed skin. This is due to increased melanin production. Risk factors here is pregnancy. You see this in middle-aged pregnant women. It’s also known as the mask of pregnancy where they get this brown to gray-brown coloration across their face, on the cheeks, on the forehead, on the upper lips.

Risk factors also include oral contraceptives, estrogen therapy, sun exposure, and darker skin types. It looks like a symmetric hyperpigmented macules or patches on the face. There’s no scales or inflammation. It’s asymptomatic. There’s no symptoms that they’re complaining about other than the discoloration. So what’s your question stem here going to look like? Well, it’ll probably be a pregnant woman because it’s just an easier place to identify.

It doesn’t mean you don’t have to be pregnant to get this, but it just tends to be more common in pregnant women. Or maybe they’re using oral contraception. With some sort of new symmetric facial hyperpigmentation, it should be pretty obvious in the question stem how you would diagnose this. This is a clinical diagnosis, although you could use a woods lamp to accentuate the pigmentation. I don’t know that I’d bother to hold on to that. Treatment number one is going to be sun protection. Number two is you could do skin lightening agents like hydroquinone, retinoids, or azelaic acid.

If you can get rid of something like the contraception, then that may be helpful. And this tends to be an ongoing issue. Vitiligo is next. This is acquired disorder causing loss of melanocytes, resulting in depigmented white skin patches. Risk factors. Autoimmune disease like thyroid disease, type 1 diabetes, pernicious anemia, family history, genetic predisposition. Clinical presentation, these are well demarcated, depigmented patches.

They have a chalky white appearance. Commonly on the face, hands. And perioral areas. Again, usually it’s like melasma. This is asymptomatic. And it’s a symmetric distribution. Your question stem here is going to be something like a progressive white patches without scales or inflammation, often in a patient with autoimmune disease.

So it’s not the same, but if you look at melasma, it is a non-inflammatory, asymptomatic facial, trying to think of how to describe this, symmetric facial hyperpigmentation. Right? So this would be symmetric facial hypopigmentation. Again, not traumatic. There’s nothing going on. There’s no itching. There’s no scaling.

Nothing like that. This is a clinical diagnosis. Again, you could use that wood’s lamp to sort of accentuate the depigmented areas. And you may consider screening for more autoimmune diseases here. First line therapy is going to be topical corticosteroids, followed by topical calcineurin inhibitors. The key here is these are for your face because they’re non-steroid immune modulators. So steroids on the skin for long periods of time can cause some bad things to happen.

Makes the skin thin out. I actually had a patient who was on long-term steroids we used to treat in my foot and ankle days who had exposed peroneal tendons because her skin had become so thin from she was actually had some asthma issues. So it was not topical steroids, but systemic steroids she was on that were just causing her all kinds of problems. But you can imagine how topical ones in the same vein applied to the same area over and over and over can cause that kind of an issue. So sun protection is important here. And again, these are associated with autoimmune disease. Great.

Now we’re going to move into chronic inflammatory and systemic issues. So acanthosis nigricans is our first one. I don’t know why. I can always picture this easier. This is hyperpigmented skin condition characterized by velvety thickening of the skin. And if you’ve ever seen images of it, which should be pretty easy for you to pull up, that’s what it looks like, like a velvety thickening of the skin. This is a marker for insulin resistance or some kind of underlying systemic diseases.

Risk factors, insulin resistance, obesity, type 2 diabetes, metabolic syndrome, polycystic ovarian syndrome, certain medications like glucocorticoids or niacin. Possibly cancer, especially gastric adenocarcinoma. And this has a higher prevalence in African-American populations, Hispanic and Native American patients. Clinical presentation. Again, that dark velvety plaque. Thickened skin texture. Common locations, and this is important because it should stand out in your test question, is posterior neck, axilla, and groin.

Just like our pigment disorders, this is usually asymptomatic. Usually there’s no scaling. There’s no itching. This has an abrupt onset. If there’s, I’m sorry, if there’s an abrupt onset or extensive disease, this might be a bigger concern for malignancy, so you want to look into that. Here the question stem would say something like an overweight or diabetic patient with dark thickened skin on the neck or axilla. It should be, again, pretty clear in the description.

This is a clinical diagnosis, although you can probably work them up for insulin resistance after you see this. And if they talk about it coming on suddenly, you may want to look into issues with malignancy. You’re going to want to treat the underlying cause, so improve glycemic control, weight loss. You might get some improvement from topical keratolytics or retinoids. And then our last topic for today, under systemic disorders that cause skin issues, is stasis dermatitis. This is a chronic inflammatory skin condition caused by venous insufficiency. You can wrap your head around this one, and I recommend that you do, because what happens here is the veins become insufficient.

What does that mean? It means that the valves in them no longer function properly. So as blood is being pushed up, let’s say from the feet into the legs, the valves that hold it from falling back down into your feet have become stretched out and weakened over time. So the blood kind of trickles back down. It doesn’t move upward in a nice column. Goes up a little, comes down a little. Goes up a little, comes down a little.

Comes down more, comes down more, goes up a little. And you get that edema in the legs because you just can’t clear the fluid. So the risk factors here are chronic venous insufficiency, which is pretty much what causes it. Varicose veins, histories of DVT, obesity, prolonged standing, older age, and heart failure. Anything that’s going to back up the venous system and make it more complicated and more pressure in there. Clinical presentation is erythema, scaling and pruritus of the lower legs, brownish hyperpigmentation. You get this like purpley brown, really dark pigmentation of the legs.

It becomes very obvious once you see it a few times. The legs often are very, are also often very swollen. It’s usually the ankles and lower legs. You can get chronic edema. You get skin thickening and ulceration. You actually get some pretty nasty ulcers from this. So this would be an older patient with leg swelling and itchy discolored skin around the ankles.

Would probably be how you would see it. You probably want to get a Doppler, an ultrasound of this. The other thing it might look like a little bit is cellulitis. But it’s in both legs and you have that edema to sort of separate it. But that’s something to think about. Treatment is compression therapy. That’s really, you have to get that fluid out.

So leg elevation, compression therapy, that kind of thing. You can use topical corticosteroids to calm down the inflammation. But we talked about why that might also be a problem long term. Emollients for skin barrier support. You want to treat the underlying venous diseases. So if someone has heart failure, for example, you want to deal with that. This is not going to be helped with antibiotics unless there’s a true infection.

Perfect. And that’ll take us to the end of this section. I actually have one more dermatology episode planned. So I’m really excited about where we’re heading, how quickly we’re getting through the material, how much we’re covering in a short period of time. But I also love how you can see the way to cover the material. I was talking with a faculty member today from a PA program. We were just talking about how just pounding more content isn’t going to help everyone.

It helps a lot of people. But some people are struggling with how to address the material, how to go through it. So just adding more, adding more, adding more all the time is not necessarily the best move. It may be the right move. But what the person next to you is doing may not work for you because they may have a different problem. You know, something you see all the time. But you have patients come in.

I work in surgery. And they’d come in. And let’s say when I was working in foot and ankle, they’d come in and say, oh, my cousin had foot surgery. And they did terrible. And then you start to dig into it. And they usually have no idea what their cousin had done. And if you get down to it, they may have something done, let’s say, on their big toe.

And you’re suggesting that on this patient, they need something done with their Achilles tendon. They’re completely unrelated. They have nothing to do with each other. But in the patient’s mind, they’re very much the same. I know I hear this a lot in spine patients. And then you dig into what they are actually trying to compare. And they’re not the same at all.

Yes, are they both surgeries on the spine? Yes, they are. But they’re not even close to the same thing. So the risks are totally different. It’s the same thing here. When you use study techniques that a friend uses, you may get great results. You may get better results than they get.

Or you may not get any results. That’s not good or bad. It’s just the way that we think. Anyway, that’s not my study tip for today. Our study tip for today, before we get into our priming question answers, is something that came up on the call last night. And I actually just put this up on Instagram, the clip of it. Because it was so good.

We were talking about ADD and getting started. And the difficulty with sitting down to study. And sitting down to do work. And getting fidgety in that first 10 minutes or so. And a couple things come up. One is that it takes about 10 to 15 minutes to get into the zone. To lock in.

To really get moving. So you have to fight through that period. You can’t leave in the first 10 minutes. Because that’s how long it takes. Now the second piece. And a student brought this up. And this is why I love doing this as a cohort.

And doing it as a group. Because on the call. A student brought up. That one of the things she does to make sure she can get to work the next day. Is come up with a plan. The night before. And as soon as she said it.

I thought. Oh. I should have shared that. It’s something I’ve been doing. It’s so powerful. I find the days when I wander around my house. And I don’t get to work.

Are the days that I didn’t have a plan. And I just don’t want to think in the morning. And come up with a plan. That’s what’s blocking me. But the nights where I sit down. And I say.

Okay. These are the three things I need to get to. I’m going to do the one. Right away. First thing in the morning. I’m going to do the other right before lunch. And I knock.

And the third one. I’ll knock out as soon as I get the other two done. Those days are easy. And I’m on fire. Right from the start. And it’s not subtle. So I was so appreciative.

That this student brought up this technique. It’s something I’ve been really pounding on. Pounding on. For about the last.

Let’s say 35 days. That each morning. Or night. I sit. And I actually physically write down. What those things are. And my days have been so much stronger.

I’ve gotten to work so much faster. I’ve had so much more energy. Getting out of bed in the morning. And closing those loops. Decreases your anxiety. And keeps you moving. So everyone wants to talk about.

Burnout. But they’re trying to treat symptoms. They’re trying to treat symptoms. Which is a big problem. In our entire culture. But the root cause. Is that you don’t feel like you’re getting anywhere.

Because you’re not. You don’t know where you want to be going. You’re not making clear decisions. About what the day holds. About what you’re trying to accomplish. So it’s impossible to know. So you just feel like you’re not making any progress.

So for all of those reasons. Today’s study tip is. Write down. Physically write them down. Don’t just think about them. Write them down. The three to five things.

That you want to get done tomorrow. And then tomorrow. Get them done. And you’ll be amazed how you feel. But not on day one. It’ll be day two. When you’re like.

Well. I feel a whole lot better. I got to work quicker. Then on day three. You’ll be like. I can’t believe this works. This seems so dumb.

When he was talking about it. And by day ten. You will not believe. What you can accomplish. And how good you feel. I know because I’m doing it.

All right. Let’s hit our priming questions. A pregnant woman develops symmetric hyperpigmentation on the cheeks and upper lip. What’s the diagnosis? This is melasma. Patchy smooth areas of hair loss appear suddenly on the scalp. What’s our diagnosis?

What’s your diagnosis? Alopecia areata. Diffuse hair shedding begins several months after a severe illness. Telogen effluvium. Thickened yellow brittle nails have not improved with topical therapy. What do you do first? Well in most cases we’re going to start oral terbinafine.

But what is going to prevent you from doing that? Why might you not do that? You’re concerned about liver issues. Itchy erythematous scaling skin with chronic swelling and around. Not under. Around the medial ankles. What’s the diagnosis?

This is stasis dermatitis. Perfect. If this episode helped you. Here’s the important takeaway. This is not about memorizing facts. It’s about how to notice and how to organize. And how to think when the pressure is on during your exams.

Remember. Think different. Work different. Score different. That’s why we don’t just teach content. That’s why we focus on skills. Because I can see people’s scores move.

If you have any questions. Or you want to look more into the notes. You can all find them at physicianassistantexamreview.com/154. We’ll take you to today’s notes. And you can find all of the notes as always on the website for all of these sections. I’ve been working on putting up some diagrams in there that are kind of fun too. You might want to check that out.

If you got something out of today’s show. Please share this with a friend. That’s how the show grows. That’s how people find out about it. That’s how people score higher. Is sharing the show. Share it with a friend.

Share it with a faculty member. Until next week. Take care. Best of luck on your exams.

More Derm for the PANCE

156 Burns, Wounds, Skin Cancer & The Study System That Exposes Your Gaps

155 Benign vs Concerning Skin Lesions – “Do I Worry?” Patterns You’ll See on PANCE

153 Desquamation, Blistering Disorders & Why Extra Time Might Hurt Your Score

151 Childhood Viral Rashes Made Simple – Exanthems, HFMD, Chickenpox & the Patterns That Show Up on PANCE

See all Derm episodes →

Get 26 Dermatology questions straight from The Final Step.

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