DERM ROTATION

Question 1

WHEAL

Answer 1

transient skin elevation that is solid, irregularly shaped, and has a variable diameter

Ex: mosquito bite or TB skin test

Special plaque composed only of fluid; Superficial area of localized skin edema

Ex: hives

Question 2

CYST

Answer 2

Elevated, encapsulated lesion usually in a sac in the dermis or hypodermis that is filled with liquid or semisolid material

Ex: sebaceous cyst

Question 3

HERPETIFORM

Answer 3

E

Question 4

SCALE

Answer 4

thin flake of dead skin

Ex: psoriasis

thickened stratum corneum (scale occurs in the epidermis)

Question 5

CRUST

Answer 5

Hard or rough surface due to dried drainage (from blood, pus, or serum)

Ex: Scab

dried fluid + keratinocytes arising from broken vesicles & bullae

Question 6

LINEAR

Answer 6

lesions follow a straight line

Question 7

ZOSTERIFORM

Answer 7

E

Question 8

EXCORIATION

Answer 8

E

Question 9

LICHENIFICATION

Answer 9

chronic thickening of the epidermis with exaggeration of its normal markings often due to scratching/rubbing

Ex: Chronic dermatitis or LSC

Question 10

ANNULAR

Answer 10

ring-shaped with a central clearing

Question 11

IMPETIGO

Answer 11

• common, contagious, superficial skin infection
• highly contagious, superficial vesiculopustular skin infection

Typically occurs at sites of superficial skin trauma (ex: insect bite)
- primarily occurs on exposed surfaces (ex: ** FACE ** or extremities)

RISK FACTORS
⦁ warm / humid conditions
⦁ poor personal hygiene

CAUSE
⦁ strep pyogenes (GABHS)
⦁ staph aureus - produces exfoliative toxin A
⦁ combo

• high incidence in children
• self limiting (will eventually go away), but if not treated = may last weeks to months

** POST - STREP GLOMERULONEPHRITIS ** - caused by group A strep
⦁ Occurring most commonly in children age 5-12 years
⦁ Patients develop symptoms 3- 6 weeks after streptococcal impetigo
⦁ Symptoms of PSGN include gross hematuria, facial edema, renal insufficiency, brown colored urine, and hypertension

PE
⦁ nonbullous and/or bullous
⦁ have vesicles and bullae containing clear yellow or slightly turbid fluid without surrounding erythema
⦁ superficial small vesicle or pustules 1-3 cm lesions
⦁ ** GOLDEN - YELLOW, HONEY CRUSTED LESION **

TYPES OF IMPETIGO
⦁ NONBULLOUS = MC type - impetigo contagiosa = vesicles, pustules = characteristic “honey colored crust”. Is associated with regional lymphadenopathy. MC etiology = ** STAPH AUREUS ** (2nd MC = GABHS)

⦁ BULLOUS = vesicles rapidly form large bullae –> lead to think “varnish-like crusts”. Have fever, diarrhea

• MC = ** STAPH AUREUS**
• this form of impetigo is rare - usually seen in newborns / young children if at all

⦁ ECTHYMA = ulcerative pyoderma caused by
** GABHS ** - heals with scarring. Not common

TREATMENT
⦁ BACTROBAN (MUPIROCIN) OINTMENT - mild = MC treatment - apply TID x 10 days
⦁ Bacitracin
⦁ Wash area gently with soap / water. good skin hygiene

If extensive disease or having systemic symptoms (fever) = systemic abx
⦁ oral abx - ** Cephalexin (Keflex**), dicloxacillin (especially effective against Staph), clindamycin, erythromycin, azithromycin, clarithromycin
⦁ In severe cases = oral antibiotics to cover for MRSA = Bactrim, doxycycline, clindamycin

Question 12

LIPOMA

Answer 12

• benign SUBCUTANEOUS tumor of adipose tissue
• soft, rounded and movable against overlying skin

Lipomas are composed of fat cells that have the same morphology as normal fat cells

MC locations = trunk or extremities

⦁  soft
⦁  symmetric
⦁  painless
⦁  easily mobile
⦁  palpable mass in subcutaneous tissue

TREATMENT
⦁ no treatment needed
⦁ may perform surgical removal for cosmetic reasons

**Some individuals have Familial Lipoma Syndrome = an autosomal dominant trait appearing in early adulthood, where an individual may have hundreds of Lipomas

A lipoma is a benign tumor composed of adipose tissue (body fat). It is the most common benign form of soft tissue tumor. Lipomas are soft to the touch, usually movable, and are generally painless.

Many lipomas are small (< 1 cm diameter) but can enlarge to sizes > 6 cm. Lipomas are commonly found in adults from 40-60 y/o, but can also be found in younger adults and children. Some sources claim that malignant transformation can occur, while others say this has yet to be convincingly documented.

Question 13

VITILIGO

Answer 13

PATHOPHYS = autoimmune mechanism - formation of antibodies to melanocytes

• autoimmune destruction of melanocytes leads to skin depigmentation
• onset = usually early in life (age 20-30)

CLINICAL MANIFESTATIONS
⦁ irregular discrete macules and patches of total depigmentation
⦁ lesions primarily occur on the face, upper trunk, fingertips, dorsum of hands, armpits, genitalia, bony prominences, perioral region, and body folds
** acral areas **
⦁ hair may be white in involved areas

- often occurs in the context of other autoimmune conditions such as
⦁	******** Pernicious anemia *******
⦁	******** Hashimoto's thyroiditis ******
⦁	DM type I
⦁	Addison's disease
⦁	SLE
⦁	Sjogrens
⦁	Myasthenia Gravis
⦁	RA
⦁	IBD
⦁	psoriasis
⦁	Alopecia areata

** Patients with other autoimmune disorders have an increased likelihood of vitiligo **

Which fungal infection may present with areas of pink or white macules, commonly on the upper torso, that may be confused with vitiligo in patients of dark complexions?

Answer: Tinea versicolor may present as pale macules that do not tan, commonly on the upper trunk.

DIAGNOSIS
⦁ usually clinical
⦁ can use woods lamp to locate areas of hypopigmentation

Workup should include laboratory tests such as thyroid function tests, hemoglobin A1c levels, complete blood count, and anti-nuclear antibody testing among others.

TREATMENT
- re-pigmentation can be achieved to variable degrees with
⦁ topical steroids = 1st line
⦁ calcineurin inhibitors ( ** Tacrolimus ** = protopic) = 2nd line
⦁ Psoralens = light-sensitive drug that absorbs UV
⦁ UVA / UVB

Calcineurin = enzyme that activates T-cells of the immune system
⦁ calcineurin inhibitor (cyclosporine + tacrolimus) = inhibits T cells - inhibits immune system

Protopic doesn’t cause skin thinning/atrophy like topical steroids, however, there is a possible link between Tacrolimus (protopic) and lymphoma

• treatment is a long process that requires patient commitment
• may need psychological support

Question 14

HALO NEVUS

Answer 14

also known as a Sutton nevus or leukoderma acquisitum centrifugum

Halo nevi = an area of depigmentation surrounding a nevi. Because of this appearance, it is described as a “halo” effect surrounding a nevus.

Halo nevi are a benign skin condition and is believed to be caused by the destruction of melanocytes by CD8+ T lymphocytes. In some cases, the pigmentation can spontaneously re-appear.

Halo nevi have not been shown to be associated with basal cell or squamous cell carcinoma.

These lesions need to be monitored regularly for any changes.

Halo nevi are associated with
⦁ Vitiligo
⦁ Turner syndrome
⦁ Malignant Melanoma

Question 15

MELASMA (CHLOASMA)

Answer 15

Hypermelanosis (hyperpigmentation) of sun exposed areas of the skin

also known as Chloasma faciei, or the mask of pregnancy when present in pregnant women)

RISK FACTORS
⦁ increased estrogen exposure (OCPs, Pregnancy)
⦁ sun exposure
⦁ women with darker complexion

⦁ Genetic predisposition is a major factor in determining whether someone will develop melasma

⦁ The incidence of melasma also increases in patients with thyroid disease

Melasma is the stimulation of melanocytes by estrogen and progesterone to produce more melanin pigments when the skin is exposed to sun.

CLINICAL MANIFESTATIONS
⦁ A tan or dark skin discoloration
⦁ Hypermelanotic (brown-pigment) symmetrical macules, especially on the face + neck
⦁ commonly found on the upper cheeks, nose, lips, upper lip, and forehead.

Although it can affect anyone, melasma is particularly common in women, especially pregnant women and those who are taking oral or patch contraceptives or hormone replacement therapy (HRT) medications

DIAGNOSIS
⦁ clinical diagnosis
⦁ wood’s lamp - appearance is unchanged under black light with dermal melasma. May be enhanced in epidermal melasma

TREATMENT
⦁ sunscreen*
⦁ topical bleachers (hydroquinone, azelaic acid, topical retinoids, chemical peels)

Melasma usually disappears a few months after child birth or stopping hormone replacement therapy.

Question 16

FOLLICULITIS

Answer 16

• superficial infection of hair follicle with singular or clusters of small papules or pustules with surrounding erythema

inflammation of the superficial or deep portion of the hair follicle

MC = Staph Aureus***

The classic clinical findings of superficial folliculitis are follicular pustules and follicular erythematous papules on hair-bearing skin

Nodules are a feature of deep follicular inflammation.

Folliculitis may be infectious or, less frequently, noninfectious (usually infectious)

Gram-negative folliculitis should be suspected in patients with acneiform lesions concentrated around the NOSE + MOUTH that are RESISTANT to long-term ANTIBIOTIC THERAPY

Gram-negative folliculitis often occurs in patients with a history of acne vulgaris who undergo long-term antibiotic therapy, as antibiotic treatment can disrupt the normal flora of the nasopharynx and allow colonization with gram-negative bacteria. Lesions tend to be fluctuant and concentrated around the nose and mouth.

FOLLICULITIS VS ACNE
⦁ Folliculitis = nothing to do with sebaceous glands or hyperkeratinization, just inflammation of hair follicle, not the entire unit
⦁ Folliculitis = not due to androgen
⦁ Folliculitis = usually more temporary

TREATMENT
- warm compresses
⦁ Topical Mupirocin** = 1st line (or BP cream)
⦁ Clindamycin
⦁ Erythromycin
⦁ oral abx for refractory / severe cases = Cephalexin, Dicloxacillin (both used for impetigo)
⦁ If MRSA suspected = ** BACTRIM ** , doxycycline or clindamycin

Question 17

HOT TUB FOLLICULITIS

Answer 17

CAUSE = ** PSEUDOMONAS AERUGINOSA **
(gram negative)

Commonly seen in people who bathe in a contaminated spa, swimming pool, or hot tub (especially if it is made of wood) ***

CLINICAL MANIFESTATIONS
⦁ small (2-10mm)
⦁ pink to red bumps - may be filled with pus or covered with a scab
⦁ appear 1-4 days after exposure to source
⦁ itchy, tender bumps located around hair follicles

TREATMENT
⦁ NONE***- reassurance! - usually resolves spontaneously within 7-14 days without treatment
⦁ oral ciprofloxacin if persistent

Question 18

PITYRIASIS ROSEA

Answer 18

• ETIOLOGY = unclear, but likely a viral source
• HHV 6 or 7**
• is self-limiting
• may have an accompanying UPPER RESPIRATORY INFECTION
• often occurs a few days after a viral illness, but can also occur more frequently in immunocompromised
• not contagious
• primarily occurs in older children / young adults
• increased prevalence in the spring/fall
• can mimic syphilis (order RPR if patient is sexually active)

CLINICAL MANIFESTATIONS
**First sign = “HERALD PATCH” (solitary salmon-colored macule on trunk 2-6cm in diameter)

–> then multiple new lesions appear a few days to 1-2 weeks later = smaller, pruritic, 1cm round/oval salmon-colored papules with white circular scaling in a ***“CHRISTMAS TREE DISTRIBUTION” on the back

• lesions are often oval with long-axis paralleling the lines of skin stress; oval, erythematous papules and small plaques
• mostly on the trunk, but may have some satellite lesions on the arm (usually proximal) - the face is usually spared
• lesions resolve in 6-12 weeks
• may be pruritic. Pruritus = MC complaint
• not contagious

ESSENTIAL CLINICAL FEATURES
⦁ discrete circular lesions
⦁ scaling on most lesions
⦁ peripheral COLLARETTE scaling*** with central clearance on at least two lesions.

OPTIONAL CLINICAL FEATURES
⦁ truncal and proximal limb distribution
⦁ most lesions appearing along cleavage lines
⦁ herald patch for at least 2 days before the rash or other lesions begin.

In many individuals with pityriasis rosea, the characteristic rash develops after vague, nonspecific symptoms that resemble those associated with an upper respiratory infection - Pityriasis rosea may have an accompanying upper respiratory infection.

Pityriasis rosea can be mistaken for secondary SYPHILIS - very similar looking rash, except syphilis also will appear on palms/soles of hands/feet

• secondary syphilis must be excluded to diagnose pityriasis rosea
• VDRL testing (venereal disease research lab test)
• FTA-Abs test (fluorescent treponemal antibody absorption = blood test - checks for antibodies to Treponema pallidum spirochete bacteria - causes syphilis)

DIAGNOSIS
⦁ A biopsy of pityriasis rosea will have extravasated erythrocytes within dermal papillae.

TREATMENT
- none needed!
⦁ if needed for pruritus = give medium potency topical steroids, PO antihistamines, oatmeal baths
⦁ Acyclovir/Valacyclovir or Phototherapy for severe cases

Question 19

WOUND ANESTHESIA

Answer 19

The maximum weight based dose of lidocaine 1% WITHOUT epinephrine = 5 mg/kg

The maximum dose of lidocaine 1% WITH epinephrine = 7 mg/kg

ex: maximum amount of 1% lidocaine without epinephrine in 3 y/o weighing 15kg
= 5 mg/kg x 15kg = 75mg
1% lidocaine = 10mg/mL = 7.5 mL

ex: maximum amount of 1% lidocaine with epinephrine in 3 y/o weighing 15kg
= 7mg/kg x 15kg = 105mg = 10.5 mL

Question 20

FROSTBITE

Answer 20

During cold exposure, vasoconstriction occurs in an effort to conserve heat. As the temperature drops below 10°C, cutaneous sensation is compromised.

With microvascular vasoconstriction, plasma begins to leak into the interstitial space. Ice crystals begin to form once the temperature approaches 0°C. Once crystals begin forming, intracellular osmolarity rises and cells begin to collapse and die.

Blood flow begins to sludge followed by stasis and cessation of flow at the capillary level. Patients will often present with pain and decreased sensation (75%) but usually do not have frank frozen and insensate tissue.

Frostbite, like burns, is classified into degrees of injury. ⦁ First-degree frostbite is characterized by anesthesia and erythema

• involves epidermis
• minimal pain with rewarming

⦁ Second-degree frostbite will have superficial vesicles surrounded by edema

• hard edema + CLEAR BLISTERS
• involves epidermis + dermis
• mild to moderate pain with rewarming

⦁ Third-degree frostbite produces hemorrhagic vesicles

• involves epidermis + dermis + hypodermis
• hemorrhagic blisters, pale grey extremity
• severe pain with rewarming **

⦁ Fourth-degree injuries extend deeper into osseous and muscle tissue.

• involves epidermis + dermis + hypodermis + muscles + tendons + bones
• no sensation - appears black / grey
• no pain = painless during rewarming

TREATMENT
- Optimal treatment should begin with removing all wet or cold clothing and assessing the patient for possible hypothermia
⦁ Any parts that are frozen should be submerged in warm circulating water (37°C – 39°C)
⦁ Warming should not be initiated until it is certain that refreezing will not occur as this can cause more tissue damage.

TREATMENT
⦁ Place hand in warm (37°C/98.6°F - 39°C/102.2°F) circulating water

Question 21

TRICHOTILLOMANIA

Answer 21

Trichotillomania, also known as trichotillosis or hair pulling disorder, is an obsessive compulsive disorder characterized by the compulsive urge to pull out one’s hair, leading to hair loss and balding, distress, and social or functional impairment.

Trichotillomania patients often eat their own hair, and may thus present with trichobezoars (hairballs) in their intestines.

The body area most affected by trichotillomania is the scalp, but hair loss is significant over all other areas of the body as well.

Habit reversal therapy is a type of psychotherapy that trains people to identify and react to the impulses that lead to their repetitive behaviors.

Women suffer more from trichotillomania, an impulse control disorder that may be difficult to treat.

OTHER REPETITIVE BEHAVIORS
Dermatophagia, which involve picking or biting the inside of the mouth, the cheeks, and the lips, often appears alongside onychophagia, and onychotillomania.

People with excoriation disorder feels an irresistible urge to pick at their skin which can lead to skin lesions, infection, and scarring

Question 22

PENICILLIN / CEPHALOSPORIN ALLERGY

Answer 22

Allergic reactions to penicillin are the most commonly reported medication allergy.

It is important to understand the actual symptoms of the reported allergy as studies have shown that up to 90% of patients with a “history” of a penicillin allergy do not have a true allergy.

True anaphylaxis occurs less than 0.01% of the time.

Cephalosporins share a similar β-lactam ring structure to penicillins and rates of cross-reactivity between the two classes of medication are reportedly between 1% and 8%. However, this risk appears to be significantly more with FIRST GENERATION CEPHALOSPORINS like cefazolin.

Additionally, the risk for allergy to cephalosporins is also more likely in patients who had a severe reaction to penicillin.

1ST GENERATION CEPHALOSPORINS
⦁	cefazolin
⦁	cephalexin
⦁	cefatrizine
⦁	cefadroxil

cefoxitin = 2nd generation
ceftriaxone = 3rd generation
cefepime = 4th generation

Question 23

HYPERSENSITIVITY REACTIONS

Answer 23

⦁ type I = the immediate development of urticaria after an ingestion

⦁ type II =

⦁ type III =

⦁ type IV =

Question 24

ISOTRETINOIN (ACCUTANE) BIRTH DEFECTS

Answer 24

Oral retinoids such as isotretinoin are used for severe acne vulgaris that is not responsive to more conservative management.

Isotretinoin is a teratogen that is very likely to cause defects if taken by a woman during pregnancy or near the time before conception

⦁	Hearing and visual impairment (blurry vision / night vision)
⦁	missing or malformed earlobes
⦁	facial dysmorphism
⦁	mental retardation 
- have all been linked to isotretinoin

Other side effects include 
⦁	psychological effects
⦁	anemia
⦁	thrombocytopenia
⦁	increased liver transaminases
⦁	hypercholesterolemia
⦁	hypertriglyceridemia

Because of the many side effects, there are strict controls on prescribing isotretinoin to women who may become pregnant.

Question 25

WHY CAN’T ISOTRETINOIN AND DOXYCYCLINE BE GIVEN TOGETHER

Answer 25

INCREASED INTRACRANIAL PRESSURE

PSEUDOTUMOR CEREBRI

Question 26

ANGIOKERATOMAS OF FORDYCE

Answer 26

D

Question 27

DISSECTING CELLULITIS

PERIFOLLICULITIS CAPITIS ABSCEDENS ET SUFFODIENS

Answer 27

DDD

Question 28

ACANTHOSIS NIGRICANS

Answer 28

• velvety thickening + hyperpigmentation of skin

- associated with
⦁	endocrine disorders 
- diabetes***
- insulin resistant syndrome - PCOS
- Acromegaly
- Cushing's Syndrome
- Addison's
- Hypothyroidism

⦁ obesity***
⦁ Paraneoplastic Syndrome - internal malignancy (most commonly GI, GU or lung) or lymphoma

Most of the cases of acanthosis nigricans are associated with obesity.

Patients with new-onset acanthosis nigricans should be screened for the presence of DM , as it is a common underlying cause.

Diabetes causes acanthosis nigricans due to stimulation of insulin-like growth factor receptor-1.

Obesity and diabetes mellitus are among the most frequently associated disorders. Rarely, acanthosis nigricans develops as a sign of internal malignancy (most commonly GI)

Abdominal adenocarcinomas, particularly gastric adenocarcinomas, represent the majority of acanthosis nigricans-associated tumors

Rarely, certain medications can cause AN = steroids, insulin, OCP, Niacin, testosterone, Aripiprazole (SGA)

⦁ Acanthosis nigricans is a potential cutaneous adverse effect of niacin (cholesterol med + vitamin B3) use due to the hyperglycemia it causes.

The familial cases of acanthosis nigricans are inherited in an autosomal DOMINANT manner

HX = insidious onset; first visible change = darkening of pigmentation

• skin changes occur slowly
• skin may also have an odor or an itch

PE = hyperpigmentation, velvety looking, skin line accentuation, surface becomes wrinkled or creased

MOST COMMON SITES = axilla, neck (back + sides), groin, antecubital fossa, knuckles

if < 40 = usually diabetes or endocrinopathy
if > 40 = should rule out adenocarcinomas of the colon
if dark thickening in the mouth = think malignancy

DIAGNOSIS
⦁ usually made clinically
⦁ biopsy = will show hyperkeratosis with melanocytes

TREATMENT
- 1) rule out diabetes
- 2) treat underlying cause - usually acanthosis nigricans will then resolve
- 3) usually no tx required for pigmentation itself
⦁ topical retinoids can be tried in patients with persistent acanthosis nigricans despite treatment of the underlying cause

Question 29

VERUCCA VULGARIS

(WARTS) - used to

Answer 29

a small, rough growth resembling a cauliflower or a solid blister

A hard, rough, skin-colored growth on the skin

It typically occurs on humans’ hands or feet but often in other locations.

Warts are caused by a VIRAL INFECTION of keratinocytes, specifically by one of the many types of human papillomavirus (HPV).
⦁ HPV 1, 2, 4 cause common warts on skin
⦁ HPV 6, 11 cause 90% of genital warts that rarely develop into cancer
⦁ HPV 16, 18 = dangerous ones - cause about 70% of cervical cancer

There are as many as 10 varieties of warts, the most common considered to be mostly harmless.

HPV infects keratinized skin, causing excessive proliferation and retention of the stratum corneum, which leads to papule formation

Infection occurs in the superficial layers of the epidermis, causing proliferation of the keratinocytes (skin cells) and hyperkeratosis — the wart

HPV is spread by direct skin-to-skin contact or autoinoculation. This means if a wart is scratched or picked, the viral particles may be spread to another area of skin. The incubation period can be as long as twelve months.

CUTANEOUS HPV
⦁ verruca vulgaris (common warts), verruca plantaris (plantar warts), verruca plana (flat warts)

MUCOSAL HPV
⦁ condyloma acuminate (genital warts)
⦁ cervical dysplasia / cancer
⦁ anogenital carcinoma (intraepithelial)

HPV has the ability to cause malignant transformation

It is possible to get warts from others; they are contagious and usually enter the body in an area of broken skin.

CLINICAL MANIFESTATIONS / PHYSICAL EXAM
⦁ firm, hyperkeratotic papules between 1-10mm with red-brown punctations (thrombosed capillaries) = food source
⦁ borders = can either be rounded or irregular
⦁ common on hands and feet

PLANTAR WARTS

• can be painful/uncomfortable if located in areas of pressure
• have black dots that are blood vessels

SUBUNGUAL / PERIUNGUAL WARTS

• a subclassification of palmar/plantar warts
• found around + under nail apparatus
• can cause nail dystrophy / pain on grasping objects
• long-standing periungual/subungual warts that have a changing morphology should be biopsied to rule out malignant transformation into SCC

FILIFORM WARTS = Filiform warts are on a long stalk like a thread. They commonly appear on the face. They are also described as digitate (like a finger).

FLAT WARTS (VERRUCA PLANA) = numerous, small, discrete, flesh-colored papules measuring 1-5mm in diameter and 1-2mm in height. Plane warts have a flat surface. The most common sites are the face, hands and shins. They are often numerous. They may be inoculated by shaving or scratching, so that they appear in a linear distribution (pseudo-Koebner response). Plane warts are mostly caused by HPV types 3 and 10.

GENITAL WARTS (CONDYLOMA ACUMINATA)
⦁	tiny, PAINLESS, papules that evolve into soft, fleshy, cauliflower-like lesions that range from skin-colored to pink/red
⦁	occur in clusters in genital regions + oropharynx
⦁	lesions persist for months, and may spontaneously resolve or may remain unchanged / grow if not treated

DIAGNOSIS

• clinical diagnosis based on appearance
• biopsy
• mucosal HPV = ** whitening of lesion with acetic acid application **

Plantar warts (HPV 1/2/4) vs callus
⦁	plantar warts interrupt skin lines
⦁	calluses - skin lines are retained

TREATMENT
- most warts resolve spontaneously within a few years, 50% will resolve within 2 years if immunocompetent

To get rid of them, we have to stimulate the body’s own immune system to attack the wart virus. Persistence with the treatment and patience is essential

⦁ cryotherapy
- ring warts commonly seen after cryotherapy - ring or donut shaped wart with central clearing

⦁ topical retinoids (adapalene, tretinoin)
⦁ Efudex

⦁ Salicylic acid - works by removing the dead surface skin cells

⦁ Trichloroacetic acid = particularly helpful for vaginal warts

⦁ electrocautery

⦁ podophyllin - a resin extracted from the root of the plant Podophyllum sp. Berberidaceae (mandrake), which contains podophyllotoxin; a cytotoxic agent that has been used topically in the treatment of genital warts. It arrests mitosis in metaphase. a cytotoxic agent - must not be used in pregnancy or in women considering pregnancy

⦁ Imiquimod (Aldara) = Topical immunomodulator - works by increasing the activity of the body’s immune system - used to treat warts (specifically works well for genital/perianal warts**), also used for AKs / superficial BCCs

⦁ Cantharidin - secreted by many species of blister beetles. It is a burn agent or a poison in large doses. It’s cutaneous effect is the separation (acantholysis) and death of epidermal cells

⦁ Bleomycin - intralesional injection - antibiotic derived from the fungus Streptomyces verticillus but is mainly used as a chemotherapy drug. It causes DNA strand scission (breakages in the DNA strand), preventing cell replication.

⦁ Candida Albicans injection - stimulates an immune response

Question 30

TINEA VERSICOLOR

Answer 30

Tinea versicolor (pityriasis versicolor) is a common superficial fungal infection.

Tinea = fungus
pityriasis = rash that causes scale/flake lesions

Patients often present with hypopigmented, hyperpigmented, or erythematous macules on the trunk and proximal upper extremities.

Tinea versicolor is a skin condition displaying hyperpigmentation as well as hypopigmentation due to infection with Malassezia species.

Unlike other disorders utilizing the term tinea, it is NOT A DERMATOPHYTE infection (trichophyton, epidermophyton, microsporum).

The causative organisms are saprophytic, lipid-dependent yeasts in the genus MALASEZZIA FURFUR.

CAUSE
- The Malassezia fungus causing tinea versicolor degrades FATTY ACIDS leading to destruction of melanocytes - which is why areas of the body that typically produce more sebum are typically affected (back / chest / shoulders)

• The degradation of lipids produces azelaic acid which damages melanocytes –> pigment changes

The yeasts produce chemicals: Azeleic Acid (used to treat acne and rosacea) that reduces the pigment in the skin

The Malassezia fungus causing tinea versicolor degrades fatty acids leading to destruction of melanocytes.

⦁ Tinea versicolor thrives in a hot + humid environment

DIAGNOSIS
⦁ clinical diagnosis
⦁ ** KOH Prep **
- The microscopic pathognomonic ** SPAGHETTI + MEATBALL ** appearance of tinea versicolor represents hyphae and spores (fungus)
⦁ Wood’s Lamp - ** yellow/green fluorescence **

The involved skin fails to tan with sun exposure

TREATMENT
- The treatment for tinea versicolor are selenium sulfide, topical and/or oral antifungal medications.

⦁	Ketoconazole (Xolegel)*** / Miconazole
⦁	Selenium Sulfide (Selsun blue)
⦁	Pyrithione Zinc (Head + Shoulders)
⦁	Nizoral shampoo
⦁	Fluconazole (Diflucan) or Itraconazole if widespread or failed topical therapy

Anti-dandruff shampoos work for tinea versicolor because same yeast is present in both conditions (Malassezia Furfur)

Azoles are delivered to the skin via sweat, so best not to shower for 8-12 hrs after oral azole therapy

Question 31

VARICELLA (CHICKENPOX)

Answer 31

Caused by HHV-3 - Varicella Zoster Virus

Chicken Pox = Primary varicella infection

Transmission = respiratory droplets, direct contact

The virus spreads mainly by touching or breathing in the virus particles that come from chickenpox blisters, and possibly through tiny droplets from infected people that get into the air after they breathe or talk

10-20 day incubation period
It takes about 2 weeks (from 10 to 21 days) after exposure to a person with chickenpox or shingles for someone to develop chickenpox

Usually lasts 5-7 days

• highly contagious!
  ⦁ is highly contagious from 2 days before onset of rash until all lesions have crusted

A person with chickenpox can spread the disease from 1 to 2 days before they get the rash until all their chickenpox blisters have formed scabs (usually 5-7 days).

RASH
- appears on face + trunk (chest / back), then spreads to extremities

• CENTRIPETAL RASH = lesions mostly distributed on face / trunk, less so on extremities
  (smallpox = centrifugal - mostly face + extremities)

⦁ vesicles - “dew drops on a rose petal” = clusters of vesicles on erythematous base
⦁ pruritic
⦁ become pustules + crust over

vesicles are in ** DIFFERENT STAGES **
- have macules, papules, vesicles, pustules, and crusted lesions

SYMPTOMS - may begin to show 1-2 days prior to rash
⦁	fever
⦁	malaise
⦁	headache
⦁	decreased appetite

• more severe presentation may occur in adults

Some people who have been vaccinated against chickenpox can still get the disease. However, the symptoms are usually milder with fewer red spots or blisters and mild or no fever. Though uncommon, some vaccinated people who get chickenpox will develop illness as serious as chickenpox in unvaccinated persons.

Chickenpox can be spread from people with shingles to others who have never had chickenpox or received the chickenpox vaccine. This can happen if a person touches or breathes in virus from shingles blisters

If a person vaccinated for chickenpox gets the disease, they can still spread it to others.

For most people, getting chickenpox once provides immunity for life. However, for a few people, they can get chickenpox more than once, although this is not common.

The best way to prevent chickenpox is to get the chickenpox vaccine. Children, adolescents, and adults should get two doses of chickenpox vaccine.

Chickenpox vaccine is very safe and effective at preventing the disease. Most people who get the vaccine will not get chickenpox. If a vaccinated person does get chickenpox, it is usually mild—with fewer red spots or blisters and mild or no fever. The chickenpox vaccine prevents almost all cases of severe disease.

TREATMENT

• usually self-limiting
• Calamine lotion and colloidal oatmeal baths may help relieve some of the itching
• Keeping fingernails trimmed short may help prevent skin infections caused by scratching blisters
• if symptomatic
  ⦁ benadryl for pruritus
  ⦁ tylenol for fever

Do not use aspirin or aspirin-containing products to relieve fever from chickenpox. The use of aspirin in children with chickenpox has been associated with Reye’s syndrome, a severe disease that affects the liver and brain and can cause death

Encourage kids/adults not to scratch chickenpox lesions, as this can lead to scarring

• Systemic
  ⦁ Acyclovir (Zovirax) = 800mg 5x/day x 7 days
  ⦁ Valacyclovir (Valtrex) = 1g TID x 7 days
  ⦁ Famciclovir = 500mg TID x 7 days

Acyclovir, an antiviral medication, is licensed for treatment of chickenpox. The medication works best if it is given within the first 24 hours after the rash starts. Other antiviral medications that may also work against chickenpox include valacyclovir and famciclovir

CDC recommends two doses of chickenpox vaccine for children, adolescents, and adults. Children should receive two doses of the vaccine—the first dose at 12 through 15 months old and a second dose at 4 through 6 years old

Question 32

DERMATOFIBROMA

Answer 32

• one of the most common benign skin growths
• due to fibrous tissue proliferation
• exact etiology = unknown
• usually occur on the extremities
• predilection for the legs

DF = seen almost exclusively in adults, and tend to occur slightly more often in females than in males

• no race predilection

CLINICAL MANIFESTATIONS
⦁ DFs can range from 2mm to 2cm
⦁ round or oval in shape
⦁ usually solitary, but may have multiple in various locations
⦁ usually small (4-5mm), firm, red or slightly purple papules that DIMPLE with lateralized pressure

The “dimple” sign is often used clinically to differentiate DFs from other growths

CAUSE
- history of possibly inciting local trauma at the site, such as from an insect bite or superficial puncture wound from thorns or wood splinters.

Dermatofibromas occur in people of all ages, although more commonly during the ages of the 20s to 40s, and develop more frequently in females than males

They are a benign tumor, although there have been cases of local recurrence, and even more rarely, distant metastases have been reported.

When considering the differential diagnosis of these lesions, it is vitally important to distinguish dermatofibromas from dermatofibrosarcoma protuberans, a similar appearing but more aggressive cutaneous neoplasm.

DIAGNOSIS
⦁ Clinical diagnosis - dimple sign
⦁ Dermoscopic evaluation of these lesions will most commonly exhibit a central white patch with a peripheral pigmented network (“starburst appearance”)

TREATMENT
⦁ NONE - benign
⦁ can excise

Question 33

DYSHIDROSIS / DYSHIDROTIC ECZEMA

Answer 33

• Cause = unknown
• Vesicular eruption on the skin of hands + feet - marked by intense itching***
• vesicles are deep
• scaling, fissures and lichenification may follow

TRIGGERS
⦁	sweating
⦁	emotional stress
⦁	warm / humid weather
⦁	pollen
⦁	metals (nickel / cobalt / chromium salts in objects and/or food)

• Association with seasonal allergies

dyshidrotic eczema blisters are known to erupt more frequently during the spring allergy season. The blisters may last up to three weeks before they begin to dry and can sometimes be large and painful. As the blisters dry, they may turn into skin cracks or cause the skin to feel thick and spongy, especially if you’ve been scratching the area

Dyshidrotic eczema usually appears in adults ages 20 through 40 but it can also affect children

People with contact dermatitis, atopic dermatitis or hay fever, are at higher risk of developing dyshidrotic eczema

Dyshidrotic eczema seems to run in families, so if you have a close relative with this form of eczema, your chance of also developing it is increased.

CLINICAL MANIFESTATION
⦁ pruritic “tapioca like” tense vesicles on soles, palms and fingers (common on lateral digits)

Characterized by a pruritic vesicular eruption comprised of clear, deep-seated vesicles without erythema erupting on the lateral aspects of fingers, the central palm, and plantar surfaces.

The eruption has been described as resembling tapioca pudding. The onset may be acute, recurrent, or chronic.

TREATMENT
⦁ High potency topical steroids - ointments preferred; may need to be given with occlusion

⦁ hydration of skin with emollient cream
⦁ cold compresses, Burrow’s solution, Tar soaks

Question 34

ROSACEA

Answer 34

Chronic acneiform disorder of facial pilosebaceous units

an inflammatory facial skin disorder characterized by erythematous papules and pustules, but no comedones.

• increased reactivity of capillaries to heat

PATHOPHYSIOLOGY
- ** dermal matrix degeneration **

• This leads to the pathologic pooling of blood and concentration of reactive oxygen species and inflammatory mediators in the dermis.

The exact etiology for rosacea is unknown. Some believe that it may be a T-cell mediated immune response to the presence of microbial agents (particularly the Demodex species, which are mites that typically infect human hair follicles). However, the evidence is conflicting

• onset: 30-50 years old
• predominantly affects females

EXACERBATING ROSACEA FACTORS
⦁ hot liquids
⦁ spicy foods
⦁ alcohol
⦁ exposure to sun + heat
⦁ exercise
⦁ stress

CLINICAL PRESENTATION OF ROSACEA
⦁ redness to cheeks, nose and chin
⦁ burning or stinging with episodes
⦁ skin dryness, edema

The nose, cheeks, forehead, chin, and glabella are the most commonly affected areas.

Clinical features include flushing, telangiectasias, erythema, papules and pustules, and rhinophyma.

More than 50% of patients with rosacea have ocular manifestations, and ocular findings may be the first manifestation of rosacea in some patients.

Variable erythema and telangiectasia are seen over the cheeks and the forehead. Inflammatory papules and pustules may be predominantly observed over the nose, the forehead, and the cheeks.

Prominence of sebaceous glands may be noted, with the development of thickened and disfigured noses (rhinophyma) in extreme cases. Unlike acne, patients generally do not report greasiness of the skin; instead, they may experience drying and peeling. The absence of comedones is another helpful distinguishing feature.

Rhinophyma may occur as an isolated entity, without other symptoms or signs of rosacea. Rhinophyma can be disfiguring

Manifestations of ocular rosacea range from minor irritation, foreign body sensation, dryness, and blurry vision to severe ocular surface disruption and inflammatory keratitis. Patients frequently describe a gritty feeling, and they commonly experience Blepharitis and conjunctivitis. Other ocular findings include lid margin and conjunctival telangiectasias, eyelid thickening, eyelid crusts and scales, chalazia and hordeolum, punctate epithelial erosions, corneal infiltrates, corneal ulcers, corneal scars, and vascularization

Ocular rosacea is most frequently diagnosed when patients also suffer from cutaneous disease. However, ocular signs and symptoms may occur prior to cutaneous manifestations in 20% of patients with rosacea

4 SUBTYPES OF ROSACEA
⦁ erythematotelangiectatic rosacea
⦁ papulopustular rosacea
⦁ phymatous rosacea (large nose - rhinophyma)
⦁ ocular rosacea

TREATMENT FOR ROSACEA

• to minimize precipitating factors
• TOPICAL ANTIBIOTICS = 1st line therapy for mild to moderate patient

use gel or creams

⦁ Azelaic acid
⦁ Metronidazole - most common
⦁ Erythromycin
⦁ Clindamycin

⦁ Brimonidine (Mirvaso) = alpha -2 agonist = vasoconstrictor; best for facial flushing / persistent redness) - brimonidine can also be used for acute angle closure glaucoma

⦁ Topical Ivermectin cream (Soolantra) = for ppl who get papulopustular acneiform rosacea due to being immunologically sensitive to mites

⦁ Laser

SYSTEMIC ANTIBIOTICS = for mod/severe rosacea
⦁ Tetracycline
⦁ Doxycycline (Oracea) / Minocycline
⦁ Erythromycin

FACIAL REDNESS/FLUSHING TX = BRIMONIDINE (MIRVASO)

PAPULOPUSTULAR DISEASE TX = metronidazole, azelaic acid, ivermectin (soolantra) = 1st line; can try sodium sulfacetamide

can do oral antibiotics for mod/severe = tetracyclines (doxy/tetra), oral metronidazole, oral ivermectin, sodium sulfacetamide

Question 35

PSEUDOFOLLICULITIS BARBAE

Answer 35

also known as barber’s itch, folliculitis barbae traumatica, razor bumps, scarring pseudofolliculitis of the beard, and shave bumps

• “razor bumps”
• very common in african americans
• occurs when free ends of tightly coiled hairs re-enter skin and cause foreign body inflammatory response
• firm papules with embedded hair

⦁ extrafollicular penetration = curly hair coming out and coming back into the hair = more common

⦁ intrafollicular penetration = hair grows out of a different spot - out of the follicle

DIAGNOSIS = made based on clinical appearance

TREATMENT
⦁ Most effective and safe is stop shaving (first line)
⦁ Laser hair removal
⦁ Adjunctive medical therapy
- Topical retinoids (Tretinoin)
- Low potency topical corticosteroids (treat only for 3-4 weeks)
- Topical antimicrobials (benzoyl peroxide 5% or clindamycin 1%)

is a medical term for persistent irritation caused by shaving

Question 36

TETRACYLINES

Answer 36

= Antimicrobial antibiotics that inhibit bacterial ribosomes- which make proteins
⦁ transcription = DNA –> mRNA
⦁ translation = mRNA –> protein (via ribosomes)

Prokaryotic Cells (Bacteria) have smaller ribosomes than Eukaryotic Cells (Humans)

Bacterial Ribosomes are made up of a 50S subunit and a 30S subunit, which combine to form a 70S ribosome

Eukaryotic Ribosomes are made up of a 60S subunit and a 40S subunit, which combine to form a 80S ribosome

Can therefore create antibiotics that selectively interfere with the bacterial ribosomes and not our own

In both Prokaryotic and Eukaryotic Cells, protein formation occurs in 3 stages of 1) Initiation 2) Elongation 3) Termination

In Prokaryotic Cells, Initiation consists of the 50S and 30S subunit combining and attaching to mRNA to form ribosome-mRNA complex
- the mRNA serves as a blueprint for the protein that is going to be synthesized

Tetracyclines were initially derived from soil-dwelling Streptomyces bacteria
- get their name from their structure of 4 rings bound together (tetra) (cyclines)

Tetracyclines bind to the A-SITE of the 30S SUBUNIT
- this inhibits tRNA from binding to the mRNA-ribosome complex, which therefore shuts down protein synthesis of the prokaryotic bacteria

TETRACYLINE ANTIBIOTICS are divided based on DURATION OF ACTION
⦁ Tetracycline = short half life (about 8 hrs)
⦁ Doxycycline/ Minocycline = longer half life (16+ hrs)

Some bacteria have developed enzymes that can break down Tetracyclines, or they have proteins on their membrane that can pump the medication out
—> developed TIGECYCLINE

TIGECYCLINE = Glycylcycline drug class = modified tetracyclines with an additional Dimethylglycocylamido side chain that prevents the medication from directly binding to the bacterial proteins so that they can overcome bacterial defense mechanisms
- was created in response to increasing resistance

TETRACYCLINE ADMINISTRATION

• topical
• oral
• Tigecycline = IV only

ORAL TETRACYCLINES should NOT be taken with food, as it can readily bind with magnesium, iron, aluminum and calcium, which makes it unable to be absorbed

• which is why Tetracyclines are NOT given to patients on iron + calcium supplements, or antacids, which can contain aluminum salts

TETRACYCLINES = BROAD SPECTRUM - meaning they can target a wide variety of both
gram + and gram - bacteria

INDICATIONS FOR TETRACYLINES
⦁ Acne
⦁ Community acquired Pneumonia
⦁

Question 37

EPIDERMOLYSIS BULLOSA

Answer 37

an inherited connective tissue disease that causes blistering of the skin and mucosal membranes

This disease is most often diagnosed in newborns and young children.

Epidermolysis bullosa encompasses a clinically and genetically heterogeneous group of rare inherited disorders characterized by marked mechanical fragility of epithelial tissues with blistering and erosions following minor trauma.