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Derm Exam 2 > Miscellaneous Dermatology > Flashcards

Miscellaneous Dermatology Flashcards

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Dermatology Board Prep flashcards
1
Q

Acanthosis Nigricans

A

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

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2
Q

Acanthosis Nigricans can be classified into 7 types:

A

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

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3
Q

Syndromic Acanthosis Nigricans types:

A

○ 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

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4
Q

Clinical Presenting Features of Acanthosis Nigricans

A

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

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5
Q

Acanthosis Nigricans management

A

○ 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

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6
Q

most common benign tumors of infancy

A

Infantile Hemangioma

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7
Q

Risk factors for infantile hemangiomas include

A

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

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8
Q

Growth Characteristics of Infantile Hemangioma

A

○ 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

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9
Q

localized vs. segmental Infantile Hemangioma

A

● 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

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10
Q

Infantile Hemangioma diagnosis

A

○ 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.

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10
Q

Infantile Hemangioma Complications

A

○ 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

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10
Q

Infantile Hemangioma Management

A

○ 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

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11
Q

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

A

Spider Angiomas

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11
Q

Spider Angiomas clinical presenation

A

○ 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

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12
Q

Spider Angiomas treatment

A

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

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13
Q

Most common type of acquired benign vascular proliferation

A

Cherry Angioma

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14
Q

Venous Lake

A

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

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15
Q

Treatment options for Venous Lake

A

Pulsed dye laser, electrosurgery, surgical excision

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16
Q

Telangiectasias

A

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

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17
Q

Treatment of Telangiectasias

A

For cosmetic purposes only
○ Light electrosurgery or Pulsed dye laser

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18
Q

Erythema Multiforme (EM)

A

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

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19
Q

Primary trigger for EM is _____

A

herpes simplex virus

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20
Q

Erythema Multiforme (EM) presentation

A

● 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

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21
Q

Erythema Multiforme (EM) treatment

A

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

22
Q

Stevens-Johnson syndrome & Toxic epidermal necrolysis

A

● 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

23
Q

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

A

Stevens-Johnson Syndrome

24
Q

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

A

Toxic Epidermal Necrolysis

25
Q

Stevens-Johnson syndrome & Toxic epidermal necrolysis pathophysiology

A

○ 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

26
Q

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

A

AIDS

27
Q

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

A

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

28
Q

Prodromal symptoms of Stevens-Johnson syndrome & Toxic epidermal necrolysis

A

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

29
Q

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

A

● 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%.

30
Q

Stevens-Johnson syndrome & Toxic epidermal necrolysis diagnosis

A

○ 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

31
Q

Stevens-Johnson syndrome & Toxic epidermal necrolysis Management

A

○ 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

32
Q

Erythema nodosum

A

● 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

33
Q

Erythema nodosum Risk Factors

A

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

34
Q

Erythema Nodosum presentation

A

○ 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

35
Q

Diagnosis of Erythema Nodosum

A

○ A punch biopsy will confirm the diagnosis

36
Q

Erythema Nodosum Management

A

○ 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

37
Q

Melasma

A

● 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

38
Q

Risk Factors for melasma

A

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

39
Q

Melasma presentation

A

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

40
Q

Melasma diagnosis

A

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

41
Q

Melasma management

A

○ 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

42
Q

Vitiligo

A

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

43
Q

Vitiligo etiology

A

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

44
Q

Vitiligo presentation

A

○ 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

45
Q

Vitiligo diagnosis

A

○ 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

46
Q

Vitiligo treatment

A

○ 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

47
Q

Decubitus Ulcers (aka Pressure Ulcers) evaluation

A

○ 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

48
Q

Staging of pressure ulcers

A

○ 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.

49
Q

Decubitus Ulcers (Pressure Ulcers) managemnent

A

○ 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

50
Q

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

A

3-4; 2

51
Q

Pilonidal Disease

A

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

52
Q

Pilonidal Disease RFs

A

○ 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

53
Q

Presenting features of Pilonidal Disease

A

○ 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

54
Q

Pilonidal Disease evaluation

A

○ 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

55
Q

Pilonidal Disease management

A

○ 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

Derm Exam 2 (5 decks)

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