Miscellaneous Dermatology

Question 1

Acanthosis Nigricans

Answer 1

Acanthosis nigricans is a localized skin
disorder manifesting with
hyperpigmented, velvety plaques
typically located in flexural and
intertriginous regions

Question 2

Acanthosis Nigricans can be classified into 7 types:

Answer 2

● Obesity– Most common
● Malignancy
● Drug-induced – (Niacin is most common)
● Syndromic (Type A & B)
● Acral
● Unilateral
● Benign

Question 3

Syndromic Acanthosis Nigricans types:

Answer 3

○ Type A refers to patients with HAIR-AN (hyperandrogenism, insulin
resistance, and acanthosis nigricans)
○ Type B is typically seen in women who have uncontrolled diabetes
mellitus and autoimmune diseases

Question 4

Clinical Presenting Features of Acanthosis Nigricans

Answer 4

○ Symmetric, dark brown hyperpigmented
plaques with a velvety appearance
● Most Common Locations:
○ Neck folds (“dirty neck” appearance),
groin and axillae

Question 5

Acanthosis Nigricans management

Answer 5

○ Correction of the underlying condition often leads to very slow resolution
○ Patients with obesity-associated AN need to be counseled regarding a healthy diet and exercise
○ May need to rule out endocrine disorders:
■ i.e. diabetes mellitus and metabolic syndrome
○ Rule out suspected carcinoma with imaging or endoscopy
○ Topical retinoids have moderate success with resolving acanthosis nigricans

Question 6

most common benign tumors of infancy

Answer 6

Infantile Hemangioma

Question 7

Risk factors for infantile hemangiomas include

Answer 7

○ Female sex, Northern European descent, prematurity, twins, older maternal age,
maternal progesterone use, placenta previa, and preeclampsia

Question 8

Growth Characteristics of Infantile Hemangioma

Answer 8

○ Usually noticed at approximately 2-3 weeks of life
○ Initial rapid growth phase usually lasts for about 1 year, with rapid growth during the first 4 months
○ This is followed by slow regression over several years, with > 90% completely involuting (shrinking) by age 10

Question 9

localized vs. segmental Infantile Hemangioma

Answer 9

● Localized- Discrete papules, nodules, or plaques that appear to arise from a central focus
● Segmental- Small or large plaques that often have many surface telangiectasias and irregular, ill-defined borders

Question 10

Infantile Hemangioma diagnosis

Answer 10

○ Doppler ultrasound can confirm the diagnosis
○ Refer any segmental, facial, or anogenital infantile hemangioma to pediatric dermatology before proliferation begins.
○ Palpate the liver in all infants with infantile hemangiomas. If palpable, or if 5 or more cutaneous hemangiomas are noted, obtain hepatic ultrasound for potential systemic involvement.

Question 10

Infantile Hemangioma Complications

Answer 10

○ Infants with greater than 5 hemangiomas are more likely to have extracutaneous lesions in the liver
○ Lesions in the “beard” distribution can be associated with airway hemangiomas.
○ Segmental hemangiomas are more likely associated with PHACE syndrome
■ Posterior fossa malformation, Hemangiomas, Arterial anomalies, Coarctation of the aorta, and Eye abnormalities
○ Lumbosacral or anogenital hemangiomas may be associated with underlying anomalies
■ Anal anomolies, abnormal genitilia, imperforate anus

Question 10

Infantile Hemangioma Management

Answer 10

○ Active non-intervention is sufficient for uncomplicated infantile
hemangiomas
● Local Therapy:
○ Topical timolol gel (preferred for superficial hemangiomas)
■ First line when warranted
○ Pulsed dye laser (used to reduce prominent redness or vessels)
● Systemic Therapy:
○ Propranolol (First Line Systemic Therapy)
■ Cardiovascular monitoring is required
○ Prednisone

Question 11

these may be indicative of underlying systemic disease, especially when found in
large numbers

Answer 11

Spider Angiomas

Question 11

Spider Angiomas clinical presenation

Answer 11

○ Bright red with a small central papule surrounded
by small radiating vessels
○ Appear on the upper half of the body, frequently
on sun-exposed areas
○ Very uncommon to occur below the level of the
umbilicus

Question 12

Spider Angiomas treatment

Answer 12

○ Typically done for cosmetic purposes
○ Treatment options include:
■ Electrodesiccation
■ Laser Treatment

Question 13

Most common type of acquired benign vascular proliferation

Answer 13

Cherry Angioma

Question 14

Venous Lake

Answer 14

● A common and benign dilation of venules
● Most often seen on the lips (especially the lower lip) & ears

Question 15

Treatment options for Venous Lake

Answer 15

Pulsed dye laser, electrosurgery, surgical excision

Question 16

Telangiectasias

Answer 16

● Permanently dilated superficial blood vessels.
● Increase in frequency with age, often due to actinic damage
● Causes of telangiectasias include

Question 17

Treatment of Telangiectasias

Answer 17

For cosmetic purposes only
○ Light electrosurgery or Pulsed dye laser

Question 18

Erythema Multiforme (EM)

Answer 18

A self-limited hypersensitivity reaction of the skin and mucous membranes characterized by the acute onset of target lesions

Question 19

Primary trigger for EM is _____

Answer 19

herpes simplex virus

Question 20

Erythema Multiforme (EM) presentation

Answer 20

● Classical target lesions are well-defined, circular, erythematous macules or papules that are less than 3 cm in diameter, have 3 distinct color zones, and a central zone that has a bulla or crust
● Lesions first appear in a symmetrical distribution on the
extremities and progress centrally

Question 21

Erythema Multiforme (EM) treatment

Answer 21

Because EM is typically self-limited, it only requires symptomatic relief
■ Topical steroids and oral antihistamines for itch
■ NSAIDs for pain
Recurrent EM (greater than 6 attacks per year) may respond to long-term
acyclovir or valacyclovir (to help suppress recurrences of HSV)
● Systemic corticosteroids are not recommended in mild cases due to HSV
because they may actually lead to continuing EM eruptions
● Reassurance is critical in these patients

Question 22

Stevens-Johnson syndrome & Toxic epidermal necrolysis

Answer 22

● Two rare, severe drug reactions that are characterized by mucosal erosions with skin pain and detachment most commonly triggered by medications ○ Considered to be the same disease along a spectrum

Question 23

Involvement of detached and detachable skin that is less than 10% of body surface area

Answer 23

Stevens-Johnson Syndrome

Question 24

Involvement of detached and detachable skin that is more than 30% of body surface area

Answer 24

Toxic Epidermal Necrolysis

Question 25

Stevens-Johnson syndrome & Toxic epidermal necrolysis pathophysiology

Answer 25

○ Investigations over the past decade have provided strong evidence that SJS and TEN are secondary to the host's inability to detoxify the culprit drug and its metabolites. This results in a cell-mediated immune response that activates cytotoxic T-cells and induces keratinocyte apoptosis via cell surface death receptor signaling

Question 26

_____ is associated with a 1000-fold increase risk of SJS/TEN

Answer 26

AIDS

Question 27

Most commonly implicated medications in Stevens-Johnson syndrome & Toxic epidermal necrolysis

Answer 27

○ Allopurinol ○ NSAIDs ○ Antibiotics ■ Penicillin, Bactrim, Ciprofloxacin ○ Anticonvulsants

Question 28

Prodromal symptoms of Stevens-Johnson syndrome & Toxic epidermal necrolysis

Answer 28

Nonspecific fevers, malaise, arthralgias / myalgias, ocular irritation, upper respiratory tract symptoms, and oropharyngeal pain. May precede skin / mucosal findings by 1-3 days

Question 29

Cutaneous and mucosal lesions of Stevens-Johnson syndrome & Toxic epidermal necrolysis

Answer 29

● Cutaneous lesions: Begin as a more typical exanthematous eruption that evolves to dusky, irregular, ill-defined coalescing macules with purpuric or detached centers. Lesions typically appear first on the central trunk, palms, and soles and then spread to the face and proximal extremities. As the disease progresses, large areas of serous blistering and sloughing may occur. Skin is typically painful and tender. ● Mucosal lesions: Oral mucosal sloughing and crusting is present in >90% of cases and ocular involvement in >80%.

Question 30

Stevens-Johnson syndrome & Toxic epidermal necrolysis diagnosis

Answer 30

○ Skin biopsy and clinical picture ○ Should order CBC with differential, urinalysis, ESR, C-reactive protein, urea and electrolytes, liver function tests, coagulation studies, glucose, magnesium, phosphate, bicarbonate, and lactate

Question 31

Stevens-Johnson syndrome & Toxic epidermal necrolysis Management

Answer 31

○ Rapid identification and withdrawal of the offending drug and transfer to an ICU or burn unit with aggressive supportive care are the most critical steps in management ■ Primary goals are to provide fluid / nutritional support, provide pain control, and monitor for infection. ○ Corticosteroids and other immunosuppressants are theoretically most beneficial in the acute, inflammatory stage ○ Necrotic epidermal tissue should not be extensively debrided. It provides a natural barrier to the environment and may promote wound healing

Question 32

Erythema nodosum

Answer 32

● Most common type of inflammatory panniculitis (inflammation of the fat) ● An inflammatory process, typically symmetrical, and located on the pretibial region ● Represents a form of hypersensitivity reaction

Question 33

Erythema nodosum Risk Factors

Answer 33

○ 50% of the time the cause or trigger is never found (idiopathic) ○ May be precipitated by infection, pregnancy, medications, connective tissue disease, or malignancy

Question 34

Erythema Nodosum presentation

Answer 34

○ Most commonly seen in a pretibial (anterior shin) distribution. Lesions are typically bilateral, but not symmetric ○ Presents as ill-defined, erythematous, tender nodules and plaques, usually 2-5 cm in diameter. They are initially bright red and slightly elevated ○ Lesions are tender, smooth and have a deep-seated appearance ○ Arthralgias are reported by a majority of patients

Question 35

Diagnosis of Erythema Nodosum

Answer 35

○ A punch biopsy will confirm the diagnosis

Question 36

Erythema Nodosum Management

Answer 36

○ Eruption typically persists for 3-6 weeks ○ Spontaneous resolution occurs in most cases ● Mainstay of treatment is symptomatic ○ Rest, elevation, and compression ○ NSAIDs ○ Colchicine ○ Potassium iodide

Question 37

Melasma

Answer 37

● An acquired disorder of hyperpigmentation typically affecting sun-exposed areas of the face ● More common in women with darker skin phototypes ● Onset most often occurs during the reproductive years in women

Question 38

Risk Factors for melasma

Answer 38

○ Hyperestrogenism (pregnancy, contraception) ○ Thyroid disease ○ UV radiation ○ Genetics

Question 39

Melasma presentation

Answer 39

○ Irregularly bordered, evenly pigmented tan macules or patches on the face ○ Patches have a "moth-eaten" appearance to their borders

Question 40

Melasma diagnosis

Answer 40

○ Typically a clinical diagnosis ○ Since pigment deposition is usually epidermal, melasma will be markedly accentuated with a Wood's lamp

Question 41

Melasma management

Answer 41

○ Strict sun protection ○ Discontinue OCPs (if possible) ○ Hydroquinone (typically first line) ○ Tri-luma (hydroquinone 4%, fluocinolone 0.01%, and tretinoin 0.05%) ○ Azelaic acid ○ Laser therapy ○ Chemical peels

Question 42

Vitiligo

Answer 42

● An acquired type of leukoderma characterized by well-circumscribed chalk-white depigmented macules or patches

Question 43

Vitiligo etiology

Answer 43

● The precise etiology of vitiligo is debated, the two leading hypotheses include: ○ Host attack on normal melanocytes (Autoimmune) ○ Intrinsic melanocyte defects (Genetics)

Question 44

Vitiligo presentation

Answer 44

○ Sharply demarcated, white macules and/or patches ○ Will generally present with symmetric involvement of the face, upper chest, hands, ankles, axillae, groin, and around orifices (eyes, nose, mouth, urethra, and anus) ○ Hair may eventually turn white (leukotrichia) ○ Will often favor sites of frequent friction or trauma

Question 45

Vitiligo diagnosis

Answer 45

○ Diagnosis can usually be made clinically ○ Wood's lamp can distinguish depigmentation from hypopigmentation ■ Under Wood's lamp, vitiligo appears "milk-white" ○ Biopsied specimens will reveal absence of melanocytes

Question 46

Vitiligo treatment

Answer 46

○ The goals of treatment include: ■ Halting progression of the disease and ■ Inducing repigmentation ● Should refer to dermatology ● First Line Treatments include: ○ Topical corticosteroids ○ Nonsteroidal anti-inflammatories (Protopic or Elidel) ■ Best used for face and genitals ○ Phototherapy (best used in combination with topical treatments) ● Excimer Laser ● Skin grafts ● Monobenzylether of hydroquinone (MBEH)- Used to achieve complete depigmentation in vitiligo

Question 47

Decubitus Ulcers (aka Pressure Ulcers) evaluation

Answer 47

○ Size, depth, presence of a sinus tract, necrotic tissue, or exudate. ○ Signs of healing: granulation tissue. Pictures are helpful while treating to track progress ○ Signs of infection: Infection impairs wound healing, treat underlying infection (warmth, erythema, purulent discharge, foul odor). Sometimes delayed healing is the ONLY sign if infection. ○ Squamous cell carcinoma can develop in chronic wounds and should always be considered

Question 48

Staging of pressure ulcers

Answer 48

○ Stage 1: Intact skin with localized area on nonblanchable erythema ○ Stage 2: Partial thickness loss of skin with exposed dermis ■ Wound is pink/red, moist, may also present as an intact blister ○ Stage 3: Full-thickness loss of skin, adipose tissue is visible. ■ Granulation tissue is often present ○ Stage 4: Full-thickness loss with exposed or directly palpable fascia, muscle, tendon, ligament, cartilage, or bone. ○ Unstageable: Full-thickness loss but extent can’t be fully confirmed because it’s obscured by slough or eschar. ○ Deep tissue pressure injury: intact or non-intact skin with localized area of non-blanchable deep red/purple discoloration. ■ Could present as a blood-filled blister as well.

Question 49

Decubitus Ulcers (Pressure Ulcers) managemnent

Answer 49

○ Stage 1: Can cover with transparent film for protection. Patient is high risk for progression! ■ Relieve pressure at the ulcer site with the aid of foam wedges, pillows, heel protectors, etc. ○ Stage 2: Semi Occlusive or occlusive dressing that maintains a moist environment. Usually don’t need much debridement ■ Avoid occlusive dressings when infection is present ○ Stage 3 & 4: Generally require debridement of necrotic tissue and coverage with dressings. ■ Necrotic tissue impairs wound healing and promotes bacterial growth

Question 50

Patients deemed to be at low risk for pressure ulcers may be moved every ____ hours, whereas those at high risk should be moved at least every ____ hours

Answer 50

3-4; 2

Question 51

Pilonidal Disease

Answer 51

infection or inflammation of the intergluteal cleft. Cause unclear although presence of hair and inflammation in the intergluteal cleft are factors. Once the sinus becomes infected, a subcutaneous abscess develops and spreads along the tract to the surface

Question 52

Pilonidal Disease RFs

Answer 52

○ Overweight/obesity, local trauma/irritation, sedentary lifestyle or prolonged sitting, deep natal cleft, increased hair density in natal cleft area, family history, characteristics of a person’s hair

Question 53

Presenting features of Pilonidal Disease

Answer 53

○ Acute ■ Sudden mild-severe pain in the intergluteal region with activities that stretch the skin overlying the natal cleft ■ Intermittent swelling or purulent/bloody drainage in the area. Fever/malaise can be present if undrained ○ Chronic ■ Recurrent or persistent drainage and pain. May have more than one sinus tract ■ Disease presenting with unusual or aggressive appearance should be evaluated for SCC with a biopsy

Question 54

Pilonidal Disease evaluation

Answer 54

○ Retract the buttock cheeks to view area of the intergluteal cleft. ○ Look for sinus tracts (looks like an opening in the skin or small hole) and drainage. ○ Look for cellulitis (often seen in acute cases) or fluctuant mass at the top of the natal cleft. ○ Imaging/lab studies not necessary

Question 55

Pilonidal Disease management

Answer 55

○ Asymptomatic ■ May rupture spontaneously. Surgery discouraged due to poor healing rates. ○ Acute ■ Prompt I&D and debridement at time of presentation- refer to surgery/ED. Will be packed with gauze and heal by secondary intention. ■ Antibiotics rarely successful alone and should be reserved for those with cellulitis ● Also in immunocompromised pts or at risk for MRSA ○ Chronic ■ Definitive treatment is surgical. ■ Recurrence rate is high between 10-55%. After healing, patients should begin regular gluteal cleft shaving/care