* Selsun Blue or Selenium Sulfide can cause Xanthotrichia or yellow hair.
* Green hair can be caused by copper in swimming pools. You can treat it with a chelating agent like topical EDTA.
* If you have allergies or are an atopic person and you have alopecia areata, your prognosis is worse than if you don’t have an atopic diathesis.
* Syphilis can cause hair loss that looks like a moth are your hair.
* Iron deficiency anemia may cause light and dark bands in your hair.
*Minoxidil (rogaine) can cause a darkening of hairs and convert soft vellus hairs to terminal hairs.
* The antimalarial chloroquine can chlorinate hair and make it lighter.
* AIDs can make black patients have straighter, softer, thinner hair.
*Pili torti is another name for twisted hair and can occur in syndromes like Bjornstad syndrmoe where there is congenital deafness (cochlear type) and pili torti.
-Hint: you can memorize it like Bjornstad makes you twist your tongue to say, just like your hair and ears get all twisted.
*Trichorrhexis nodosa is a condition where it looks like there are two broomsticks smashed together. They can split, and this is why you should be careful while straightening your hair!
*Trichoptilosis is the medical word for split ends. (Isn’t it amazing that we have to study this?!)
* Trichorrhexis Invaginata is the bamboo hair where the hairs invaginate on themselves. It is strongly linked with Netherton Syndrome.
*Sometimes kinking hair can be a sign of impending male-pattern hair loss! Beware. So are whisker hairs!
*Fetal Alcohol Syndrome can cause hypertrichosis (too much hair), small faces, hemangiomas, and mental and physical retardation. Don’t drink while Pregnant!!!
*If all of a sudden you get a bunch of fine baby hairs or Acquired hypertrichoisis languginosa rule out internal malignancy.
*Oral steroids, Cyclosporine, Minoxidil, sterptomycin, penicillamine, PUVA can all cause hypertrichosis.
* Selsun Blue or Selenium Sulfide can cause Xanthotrichia or yellow hair.
I was on a flight one day next to a pediatrician and we got to talking about interesting derm cases she had seen in her life. One of the cases she spoke about was this child who needed to have a procedure for his pulmonary AV malformation. She said she later read up about it and went back in to ask her patient if he ever suffered from nose-bleeds? The patient stated he had and so had many members of his family. Eventually, the pediatrician figured out that it was Osler-Weber-Rendu Syndrome.
Apparently, talking to strangers on a flight paid off a bit for me on my first day of dermatology residency! I had a patient who had a bloody nose (epistaxis), which apparently happened to her a lot since early childhood. My attending started checking her fingertips, palms, soles, face for telangiectasias. He also checked her oral mucosa, lips, nose, eyes for them as well. Although, she didn’t have any, it was an interesting way to think about nose bleeds that brought up this syndrome.
Osler-Weber-Rendu Syndrome is also known as Hereditary Hemorrhagic Telangiectasia Syndrome. Just as the patient above had all his family members involved, OSWR syndrome is inherited in an autosomal dominant (AD) pattern with the gene locus being 9q33-34. It is caused by a mutation in endoglin (a TGF-B binding protien on endothelial cells). Its incidence is about 1-2 in 100,000 people, affecting both men and women equally. Initially, it presents with childhood nose bleeds in half the patients and in the 3-4th decade, cutaneous telangectasias are seen.
Just like other genodermatoses, it can affect different organ systems. In the GI, it can casue hemorrage 2/2 to telangiectasias. It can casue AV fistulas in the lungs, like the first patient I talked about.
You would want to order a CXR to screen (then an MRI), CBC, stool guaiac initially.
You want to make sure these patients are seen by an ENT regarding their nose bleeds and possibly GI and or thoracic surgeon depending on symptoms. Life threatening bleeds and complicated pulmonary AV fistulas will worsen prognosis.
DDx: CREST, ataxia-telangectasia, Fabry’s, generalized essential telangiectasia.
Drugs that cover Pseudomonas
*PCN Class- Piperacillin/Tazobactam (Zosyn)
*Cephalosporin Class- Ceftazidime-3rd generation (which only covers gram negatives) and Cefipime-4th generation
*Fluoroquinolones-Levafloxacin (Levaquin) and Ciprofloxacin
*Carbapenems- Doripenem, Imipenem, Meropenem
Thank you Michael Trillanes (Pharmacy Student!)
Drugs that cover MRSA
*Tetracyclines- Doxyclicine, Minocycline
*Daptomycin (but not PNA, plus it causes eosinophlic PNA)
*Ceftaroline -5th generation Cephalosporin
*Rifampin (if used in combination)
Thank you Jennifer Phan (Pharmacy student!)
Erythema Ab Igne or Toasted Skin Syndrome is persistent reticulated erythema that is produced by long-containing exposure to excessive heat without the production of a burn. It starts as mottling caused by local hemostasis, that progresses to a reticulated erythema and pigmentation After the cause is removed, the pigmentation may gradually disappear, but in some cases it is permanent
Histologically, there is thermal elastosis where there is more elastic tissue in the dermis that is simliar to actinic elastosis.
It has been reported in various case reports becasue of computers lying on people, heaters, fireplaces, radiators, heating pads, etc.
There has been rare cases where the epithelial atypia is noted and Bowen’s disease.
Remove the causative agent. 5-FU creams may help in reversing this alteration in the epidermis. Bland emollients may help in treatment. Klingman’s combo of 5% hydroquinone in 0.1% retinoic acid and 0.1% dexamethasone may help the pigmentation.
It is almost summer and with summer comes fun in the sun and not so much fun with sunburns. I thought it would be a good time to talk about the various type of burns and dust off the Andrews book for all you derm people!
Changes in Skin resulting from dry heat are classified with 4 degrees.
For those sun worshipers out there, the most common type we will see is a first-degree burn of the skin in which the skin appears red and there is peeling. Basically here, there is an active congestion of superficial blood vessels causing erythema and subsequent desquamation of the epidermis.
Second Degree Burns are subdivided into superficial and deep forms. Superficial form involves serum leaking out of the capillaries which has vesicles and bleps under the epidermis. It can heal without scaring. The deeper form of second degree burns involves the reticular dermis which destroys appendages and compromises blood flow, requiring 1 month to heal with scarring Deeper 2nd degree burns don’t hurt and are pale, while superficial 2nd degree are painful like 1st degree.
Third Degree Burns involves full thickness loos of skin and sometimes the subQ, there is no epithelium to regenerate, so you get an ulcerating scar wound
Fourth-degree destroys the whole skin and subQ fat, along with tendons. Like third degree, these require skin grafts. Both 3rd and 4th degree, cause consitutional symptoms.
Shock may occur within 24 hours of burn, along with toxemia from the absorption of the destroyed tissue. Poorer prognosis with more involvement of the body, sepsiscellulitis, electrolyte/fluid imbalances may occur Scarring may produce deformitises and there may be delayed postburn blistering, along with the development of sarcomas and carcinomas.
Prompt COLD water applicationice water until pain resolves. For 2nd degree superficial, don’t rupture vesicles/bullae because you want the skin barrier intact. If the blisters are too tense, use a steril eneeder to collapse the blister Collagen-synthetic bilaminate membrnes are being used now as skin substitutes. Abx, fluids, good nutrition to prevent morbidity and mortality from bacterial/fungal infection.
Electrical burns can be either flash or contact burns. Lighting burns have an entrance and exit wound, can be lethal if it causes internal injuries such as cardiac arrest. These burns may cause a christmas treearborizing pattern that is pathogmonic
Hot tar burns: Just know neosporin contains polyoxyetheylene sorbitan that may remove the hot tar from the burn
Don’t forget the rule of 9s for burns
Necrobiosis Lipoidica (NL) is a disorder of collagen degeneration with a granulomatous response, thickening of blood vessel walls, and fat deposition that we predominately see in diabetics as more than 50% of patients with NL are insulin dependent. In fact, it used to be called Necrobiosis Lipoidica Diabeticorum. It can often precede the onset of diabetes in some patients. It commonly affects patients in the 3rd-4th decades of life, mostly in females, and mostly on the anterior lower legs.
The course of NL stars with an oval, violaceous patch that expands with an advancing erythematous border with central yellow-brown. This center atrophies and has a waxy surface with prominent telangectasias. Ulceration can occur usually after trauma.
Diagnosis can be made clinically or with biopsy.
Treatment includes topical and intralesional steriods to arrest the inflammation, but may also worsen atrophy. Therefore, some solutions are diluted to avoid this side effect of steroids. Systemic steroids, Pentoxifylline may also be used. Alternatively, low dose aspirin and dipyridamole can also be used. One of the theories behind necrobiosis lipoidica is a microvasculature change in the dermis causing an immune complex-mediated vasculitis with vascular occlusion in the small vessels with a tendency towards platelet aggregation. Therefore, aspirin and dipyridamole may help inhibit platelet aggregation which will help with the ulceration of lesions themselves.
Yesterday, I was fortunate to go to dermatology journal club and when it was over, our program director gave us this sheet of 10 rules to be successful according to Investor’s Business Daily. I wanted to share them with you all because the way he described it was so inspiring. I feel so lucky to have a program director that not only wants us to learn our dermatology, but cares to help us acheive the most out of our lives. He is my “John Wooden” , a coach not only on the courts, but in life…haha… and I wanted to share his messages, and sorry, if this sounds like an after-school special.
1. How you think is everything- think positive. Everyday in life, we are flooded with circumstances that are less than ideal, but instead of focusing on that, be excited about what is good about those circumstances. If anything, bad circumstances make you stronger. Focus on the positive. Do this with people too, people can be pretty nasty sometimes, but if you focus on what is good about them, what you can learn from them, you won’t be filled with negative energy. It is very easy to get caught up in it, but try to see the good.
2. Decide upon your true dreams and goals. They suggest writing down what you want in life. If you want to run a marthon, write that down somewhere, and think about a plan on how to get there. I think being sure enough about your dreams to literally write them down is the first of many steps to get your goal.
3. Take Action! Goals are nothing without action, put the work into it. If you want a dermatology residency, contact residents, read your dermatology books, write papers. Do something about it.
4. Never stop learning. We feel better about things that we know about, and we know about them by studying. Sometimes it is tough to get motivated to study, I feel the senioritis myself, but you really have keep learning!
5. Be persistent and work hard. Success is a marthon, not a sprint. You don’t know how many times I have called my dad crying and that is what he says. It is true, sometimes the journey is not always smooth sailing, you can’t give up…you have to keep at it.
6. Learn to analyze details- get all the facts, all the input. Learn from your mistakes.
Sometimes you can’t achieve a goal on your own, you need help, you need to know what you are up against.
7. Focus your time and money- we have only limited resources, so use them wisely. Don’t waste your time in dead-end situations, spend it in situations that are worthwhile. My program director told me, there are these specific windows of opportunity in life, recognize them because they are there for only a limited amount of time.
8. Don’t be afraid to be innovative. There is no one way to achieve anything. When I was applying to dermatology, nobody said, hey make a website you will get in. I made a website because I loved dermatology and it was my way of “writing it down on paper” to remind myself, I still wanted and loved it. I think it kind of helped me achieve my impossible goal. Sometimes doing what you love will allow you to be more creative than the next guy in achieving your goal. Be yourself, you don’t have to fit into a mold, and you will get it.
9. Deal and communicate with people effectively- you can’t do this on your own. You need to interact with others, and do it in a way where you help them bring out their strengths and in doing so, you will bring out your own.
10. Be honest, dependable, and take responsibility. Otherwise 1-9 won’t matter.
In medicine, we are constantly tired, stressed out, and overworked. Do your end of deal, be honest, be a good person, because your achievment will mean nothing if you aren’t a good person at the end of the day.
Also, something that kind of fits into this whole dream big, is there will be people along the way that will discourage you. That unfortunately comes with the territory of having a dream or asserting yourself in any way. You have to believe in yourself and believe in your dreams and ignore the backlash. Sometimes these “nay- sayers” can be in your own family, but you still have to keep going for what you want. Respectfully disagree and achieve it!
Ok, hope that motivates some of you. I know it’s cheesy, but I truly believe it. GOOD LUCK!
Dear loyal readers,
I wanted to share my happy news with all of you that I got into dermatology and will start my residency in Southern California starting in July 2012! I cannot be more thrilled and am especially grateful to be working with amazing mentors! I have really appreciated all the support of my friends and family (and new friends!) for reading my website and letting me examine their skin and watching my face light up when I talk about things like botox. This was an aspiration I never thought in my wildest dreams would come true and I truly believe, if it could happen for me, whatever your dream is will happen for you if you don’t give up!
If you are a dermatology applicant going through this, definitely feel free to comment and I will try to help you through it!
Thank you so much from the bottom of my heart for your support!! I love you all!
Pseudoxanthoma elasticum (PXE) is an inherited defect in the elastic tissue which results in calcification and fragmentation of elastic fibers that causes systemic manifestations. This syndrome has flexurally distributed yellow papules (pseudoxanthomas) which can be associated with HTN, claudication, GI bleeding, angiod streaks in ocular fundus/blidness. This disease is typically diagnosed in the third and fourth decade of life (although can begin at a much younger age) with a prevalance of around 1: 160,000. PXE is thought to be genetic with both autosomal dominant and autosomal recessive inheritance patterns; it affects females more than males though with a 2:1 ratio.
Skin lesions themselves are numerous, tiny yellow papules that are arranged in lines in flexural areas like the neck and the axilla. It may also affect antecubital/popliteal fossa, inguinal, periumbilicial areas and inner lower lip (mucosal surfaces). Some describe PXE as the skin of a plucked chicken and in some cases skin may appear folded and lax.
Angiod streaks happen in over 80% of patients with PXE. Angiod streaks are red-brown bands that look like irregular blood vessels that are almost always bilateral. Another area that is involved is the brunch membrane. The Brunch membrane is a collagen- and elastin- containing membraine between the retina and the choroid that may be degenerated in this conditon. Retinal changes are usually seen after age 20 and they may be the only sign of disease, bilndness in some form is common, but complete blindness is rare. One of the pathognomonic findings in PXE is a peau’ d orange caused by changes in retinal pigmented epithelium overlying a calcified and degenerating Bruch’s membrane.
However, angiod streaks, which are common in PXE can also be found in sickle cell anemia and paget’s disease.
Calcification of internal elastic lamina causes accelerated atherosclerosis. HTN, angina, MI, diminished arterial pulses, intermittent claudication can also occur. If a patient has an MI without other signs of atherosclerosis, think about PXE.
Yellow papular lesions can be found on gastric mucosa and bleeding can cause fatalties.
Diagnosis of PXE: You don’t necessarily have to have skin lesions to think about PXE, you can do a nonlesional skin biopsy in the flexural skin and establish the diagnosis. You will see calcification/fragmentation and clumping of elastic fibers in deep dermis or in scars in normal skin which is considered the gold standard for diagnosis. It is recommended that fundoscopic examinations be performed in all patients that you are suspecting.
Gene Defect: ABCC6, Involves the MDRP (multiple drug resistant protein).
Today, we had a patient come in to our clinic with this rash that came on after he had a “head cold” a week prior to the eruption of the lesions. It started off with one large patch with some scale on it on his left shoulder which spread to his abdomen and back. His lesions were minimally itchy, only noticeable when he scratches them.
PItyriasis Rosea (PR) is an acute exathmeatous eruption that can occur after an URI and is commonly seen in a pediatric population. It normally starts (around eighty percent of the time) as a single, primary “herald” patch/plaque and 1-2 weeks later a generalized secondary exanthematous eruption occurs. Age of onset is typically between 10-43 years of age, but can be seen in other age groups. More commonly, it occurs in the spring and fall. Our patient fit in both the age and the timing. The etiology is a form of herpes 7. The degree of pruritis in PR varies with around half of patient complaining of mild pruritis, 1/4 of no pruritis, and the other 1/4 complaining of severe pruritis. The classic herald patch is an oval slightly raised plaque with a fine colarette scale, that you can appreciate above. The exanthem itself involves fine scaly, papules/plaques that are typically salmon colored. The distribution of PR is interesting, in that it is said to be in a “christmas tree” pattern in the trunk and proximal arms. Our patients lesions were mainly concentrated on abdomen, rather than back with no facial involvement. Atypical PR may involve lesions present only on face/neck.
Dermatopathology reveals a patchy, or diffuse parakeratosis, no granular layer, acanthosis, focal spongiosis, microscopic vesicles. Occasionally dyskeratotic cells can be appreciated.
Treatment: Antihistamine if needed, but for the most part this is self limiting within 6 weeks. If it doesn’t start to resolve, consider biopsy.