DermGunner

In medical school, we learn many mnemonics meant to make anatomy easier.

SCALP is the one we use to remember the layers of the scalp.
Skin
Close connective tissue, cutaneous vessels/nerves
Aponeurosis
Loose connective tissue/ DANGER ZONE
Pericranium/periosteum of the skull bone

(note: loose connective tissue is not included in the picture above)

Facial nerve anatomy is also a big topic when doing surgeries involving the face. In pediatrics, it is important when you evaluate babies for facial assymetry. In neurology/primary care settings, it is critical for understanding Bell’s Palsy. The facial nerve is the 7th of the 12 cranial nerves and it emerges from the brainstem between the pons/medulla and controls facial muscle expressions, taste from the anterior 2/3 of tongue/oral cavity, and supplies parasympathetic fibers to head/neck ganglia. The branches are very important for facial surgeons and dermatologists and we use many mnemonics to remember them. The one I learned at Michigan State University was Two Zebras Bit My Cookie.
Two= temporal
Zebras=zyogmatic
Bit= buccal
My= mandibular
Cookie= cervical branch.
All of these branches of the facial nerve exited from the parotid gland.
Other mnemonics include “Today Zoey bummmed by car, To Zanzibar By Motor Car, Tell Ziggy Bob Marley Called”…etc, etc.
Some people include the posterior auricular nerve and remember “Perhaps a Tiny Zebra bit my cheek” or “Please tell Ziggy Bob Marley Called”

Facial muscles are also very important to understand.  In the days of botox and dermal fillers, it is important to know what anatomy lies in the areas you inject. 

To start learning this, it helps to understand the rounder muscles “orbicularis” have to be around the rounder parts of your face like your mouth and eyes.  The rest of the anatomy makes sense if you think of the underlying bone or the purpose of the muscle. 

Hope that helps to scratch the surface of basic anatomy, now we will move on to the layers of the skin. 

In terms of skin itself we think of the three major layers: epidermis, dermis, subcutaneous fat/tissue.  Skin is thicker on the dorsal and extensor surfaces, but thinner on the ventral/flexor surfaces.  We will hit upon the first two layers in more detail. 

EPIDERMIS

The epidermis is the top layer that is composed of stratified squamous epithelium.  Note that epidermis thickness varies based on where it is: palms/soles it is 1.5mm thick on average, whereas eyelid epidermis is around .05 mm.  Epidermis typically has five layers: Stratum corneum, stratum lucidum, stratum granulosum, stratum spinosum, stratum basale.  The mnemonic I learned is Cher Likes Getting Some Botox.  Some people have told me that they believe the lucidum layer is the third layer instead of the second and they remember California Girls Like String Bikinis.  The lucidum layer isn’t always present depending on the thickness of the skin.  Three branched cells in the epidermis include: melanocyte (which makes melanin), Langerhans’ cells (immune cells), and Merkel cells (unknown function).   

From bottom to top, you can think of the basal cells dividing to form keratinocytes/prickle cells that comprise the spinous layer.  The spinous layer is connected with intracellular bridges and compose an insoluble protein that eventually becomes part of the stratum corneum.  As cells flatten as they move up, their cytoplasm becomes granular as in the stratum granulosum and they finally die when they form the basket weave structure on histopathology of teh stratum corneum. 

DERMIS

The dermis is thicker in the back up to 3.0mm, and thinner on the eyelid at .3mm just like in the epidermis.  It is composed of three types of connective tissues: collagen, elastic tissue, and reticular fibers. It has 2 layers, rather than the 5 of the epidermis.  The upper layer is the Papillary Layer and the lower layer is the Reticular layer.  The papillary layer is composed of thin, haphazardly arranged collagen fibers, wehreas teh reticular layer has thick collagen fibers that are arranged parallel to the surface of thse skin.   Histocytes are wondering macrophages in this layer that accumalate hemosiderin, melanin, and debris.  Mast cells are also in this layer and release histamine and heparin around blood vessels.  The dermis is important for touch/pressure sensations derived from Meissner’s and Vater-Pacini corpusles.  Low intensity stimulation causes itching sensations, whereas higher intensity causes pain/inflammation.  Scratching converts intolerable itching to tolerable pain, which is why people scratch.   The dermis is important carrier of nerves, hair follicles and hair erector muscles, apocrine glands/eccrine glands. 

The distinction between the dermis/epidermis is an important one for many reasons.  In terms of basic nomenclature, an erosion is a focal loss of only the epidermis and therefore doesn’t scar.  However, an ulcer penetrates to the dermis and does scar.

Subcutaneous Tissue

Earlier we talked about Erythasma caused by Corynebacterium minutissimum. Today, we will talk about a condition caused by a related Corneybacterium tenuis. Trichomycosis Axillaris is an axillary/pubic hair infection in which tiny colonies of  bacteria coat hairs and cause an unpleaseant odor. The affected hair appears as if it has been covered with a colored powdered sugar (but instead it’s really just the bacteria). Normally, the condition in symptomless with the exception of feeling sweaty and foul-smelling. Using microscopy, you can rule out lice and hair casts. Treatment incudes hair removal with shaving, deodarants/antibacterial soaps, and disinfecting solutions. Topical antibiotics like erythromycin may also be used, just like in erythasma. Rare complications of this condition, could be bacterial destruction of the hair follicle, so be aware of this!

Erythrasma

Erythrasma is a bacterial infection that can be confused with tinea cruris when in the groin, since it too has the half-moon shaped plaque.   It is also in the differential of other intertriginous conditions.  It is uniformly brown and scaly.  It is caused by the bacteria  Corynebacterium minutissmum (gram + rod) that produces porphyrins which fluouresce coral-red with a Wood’s light, that differentiates it from tinea cruris which will not.  The most common site of erythrasma is in the fourth interdigital toe space, but also seen near the groin, inframmary folds/axilla.  Gram stain will show gram + rod organism in filaments which you may want to obtain by using a clear tape to the scale.  Superinfection with candida or fungus is known to occur. 

TREATMENT

Erythromycin or clarithromycin, topical miconazole, clotrimazole, econazole may work.  Clindamycin topical for acne may also work.

Pityriasis Lichenoides is a rare disease with a chronic and acute form.  It can be often mistaken for insect bites or varicella. 

PLEVA or pitryiasis lichenoides et varioliformis acuta or Mucha Habermann disease is the acute form; whereas PLC of pitryiasis lichenoides chronica is the chronic form.  Both PLC and PLEAVA are part of a group of T-cell lyphoproliferative disorders.  Both diseases are more common in males in middle ages, rare in the elderly/babies.  Although, there is no definitive cause of Pityriasis Lichenoides, there are three theories that may account for it.  One is an  inflammatory processes in response to infection;The second is a benign T-cell lymphoproliferative disorder; finally is an immune complex hypersensitivity vasculitis. 

PLEVA

Benign self-limited papulosquamous disorder that begins with mild itching and a low-grade fever, after developing crops of round reddish-brown papules on the trunk, thighs, and upper arms.  Palms and soles may be involved in rare cases.  Lesions may have a violaceous center and surrounding erythematous rim with micaceous (thick) scale.  A high grade fever is a rare complication that may be associated with the ulceronecrotic type of lesion.  Arthritis and superinfection may also be complicating factors. 

PLC/Juliusberg Type

Generalized pink papules that progress into brownish papules with fine, micalike scale that is only obvious when scrtched, without systemic symptoms in the same distribution as PLEVA.   PLC is less symptomatic than PLEVA. 

TREATMENT

Erythromycin taken orally at dosages of 30 to 50mg/kg/day that is tapered over months.  PUVA/UVB phototherapy can also be implemented.  I personally have seen tetracyclines used for cases.  Methotrexate, oral corticosteroids, dapsone can also be used.

Malignant Melanoma is a malignancy of melanocytes that can occur in the skin, eyes, ears, GI tract, leptomeninges, or any of the mucosal surfaces. It can metastasize even to the brain and heart.

Risk factors: lifetime risk was 1/50 in 2010, highest incidence in Australia/New Zealand. Median age of diagnosis is 53 years of age, MCC cancer in women 25-29. UV radiation, sunburns are a risk factor.
SunBurns are due to UVB and UVA radiation in the form of UVA of sunbeds and psoralen and PUVA therapy are all risk factors. The latter two are used in treatment of conditions like MF, Vitiligo, Psoriasis, Eczema. People who sunburn easier than suntan have a 2-3 increased risk of getting melanoma. Also, interestingly, continuous UV radiation can be protective compared to intermittent/vacation sun exposures. The reason for this counterintuitive fact is thought to be related to chronic sunlight causing immunosuppression.

Sunscreen Effectiveness: sunscreens block UVB better than UVA (which is up to 95% of UV spectrum). UVB sunscreens are not as good as UVA in preventing melanoma. Sunscreens containing zinc oxide or titanium dioxide reflect light and act as physical sunscreens to block UVA better.

ABCDEs of MM include assymetry, border irregularity, color variation, diabeter enlargment, evolution. Ulceration/bleeding are late signs.

Red, White, Blue of Melanoma
Redness in melanoma indicates vasodilation and inflammation, whereas white indicates regression/inflammation, blue indicates deep pigment in the dermis/depth of tumor.

4 major clinical-histopathological subtypes
1. Superficial Spreading Melanoma (SSM)
2. Nodular Melanoma (NM)
3. Lentigo Maligna Melanoma (LMM)
4. Acral Lentiginous Melanoma (ALM)

SSM includes 70% of melanomas, usually with a diameter greater than 6mm, occuring in the trunk of men/women and legs of women. They begin as flat brown lesions that spread radially and regress (irregularly shaped) and clasically become a combo of colors diversifying more as time proceeds.

NM accounts for 15-20% of melanomas on trunk and legs, with very rapid growth in weeks to months, described as a brown to black papule/nodule that bleeds and ulcerates. NM can be misdiagnosed as a SK, DF, hemangioma, blood blister.

LNM accounts for 4-15% or melanomas occuring in sun-damaged skin (like lentigos) on head, neck, arms, average age of 65. It grows slowly for years with a precursor lesion that is large and existing for years. LMN may ulcerate and enter a tumor stage where prognosis is dependent on depth of tumor.

Acral Lentiginous Melanoma: 2-8% of melanomas in whites, but the majority in African Americans, asians, hispanics occuring on glabrous areas like palms/soles. A sudden appearance of pigmented band at the proximal nail fold is suggestive of melanoma and the periungal spread of melanoma to proximal and lateral nail folds is called Hutchingson’s sign (recall Hutchington distribution for herpes zoster or Hutchington teeth for congenital syphillis).

This weekend I volunteered at a local Harvest Festival to help with basic medical screenings including accuchecks, BP checks, vision checks, feet exams, and skin exams. Of course, I was all over the skin exams and although, for the most part, I only saw very common entities like acne, SKs, idiopathic guttate hypomelanosis and benign nevi, I was able to see something I had only read about before. 

I had a 50 something- year-old Caucasian male with multiple erythematous plaques with surrounding fine white collarette scale scattered on the sun exposed upper and lower extremities.  At first glance, I was convinced that this represented actinic damage in the form of AKs and SCCs.  However, I noticed there was no facial involvement, it was only on the upper and lower extremities and I figured if this man had such diffuse actinic damage, that he would have had some lesions on his face or ears.  Luckily, I had the help of a friend who also loves dermatology who had said she had a similar case of a patient that seemed to have actinic damage, but it turned out to be an entirely different entity called Disseminated Superficial Actinic Porokeratosis or DSAP. 

After googling it, I stumbled upon some blogs of patients that were so frustrated that their dermatologists/primary care physicians had missed this diagnosis and had called their condition something else or biopsied to call it “nothing”.  So what was this mysterious condition?

Disseminated Superficial Actinic Porokeratosis (DSAP) is an autosomal dominant condition first discovered in Texas initally characterized by multiple follicular keratotic brownish-red papules with rasied borders that enlarge peripherally, leaving depressed centers.  These central depressed centers may look like dells, follicular plugs, or scaly lesions.  Typically, DSAP is found on sun exposed areas, most commonly in women in their 30s-40s of European descent usually arising in the summer time. Lesions of DSAP typically do not sweat, but they may itch, especially if exposed to the sun. 

Histology of DSAP according to NZ dermnet porokeratosis in general involves: a  hyperkeratotic lesion with a discrete parakeratotic column at the margin. The diagnostic feature of porokeratosis is a cornoid lamella which represents a raised margin of the lesion, which is a  parakeratotic column overlying a small vertical zone of dyskeratotic and vacuolated cells within the epidermis.  A  focal loss of the granular layer and increased lymphocytic infilatrate may also be appreciated.

Treatment isn’t ideal, but can include: cryotherapy (which may be very tedious in a patient with many lesions), 5-flourouracil creams, Imiquimod (Aldara), AHA creams, Calcipotrein, photodynamic therapy.  Prevention with sunblock and sunprotection is recommended.

Take Home Message: DSAP is a condition we should think about when we see the picture above, although the treatment is similar to that of AK, it is a different entity that histologically is a porokeratosis. 

Take Home Message 2: You can learn good dermatology when you least expect it, so keep your eyes open and your smartphone near!

Henoch Schonlein purpura is a condition in which there is a palpable purpura of the lower extremities with at least one other feature. In total, I used to learn HSP with the abberviation “AR-AR”: Abdomninal pain that is diffuse, Renal problems like hematuria/proteinuria with IgA deposits in glomeruli, Arthralagias, and Rash (palpable purpura). According to the Journal Watch July 2011 by Medicis, the first ase of HSP is reported after the flu vaccine in Japan.
In short within 2 days after the vaccine, patients developed symptoms of HSP. Luckily these patients either experienced spontaneous resolution of their symptoms or were treated successfully. The study did not prove a causal relationship between influenza vaccine and HSP, but did suggest it was something to think about.

An article in Journal Watch June 2011 put out by Medicis talks about treating tinea capitis, a fungal infection on the skin comparing two common treatments.

Since the 1950s, they state that griseofulvin was the treatment of choice in children because of it’s safety/price; however, it requires a long tx up to 8 weeks and is absorbed inconsistently. Treatments like terbinafine or the -conzoles have been used recently, but are more expensive and usually limited to adults.

Although, studies were unable to show a significant difference in efficacy between the two, they did make recommendations for targeting certain types of fungi. The conclusion was to use Terbinafine for Trichophyton species and Griseofulvin for Microsporum species. (think: T for T).