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Pathology 1 > Skin Pathology > Flashcards

Skin Pathology Flashcards

1
Q

What are the 5 layers of the Epidermis?

A
  1. Stratum Basale
  2. Stratum Spinosum
  3. Stratum Granulosum
  4. Stratum Lucidum
  5. Stratum Corneum
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2
Q 
Describe the gross appearance of Vitiligo.
What populations does vitiligo affect?
Are there any predisposing factors?
What is the etiology?
Microscopic Appearance?
A

Irregular, completely depigmented patches
Common and may affect any race
Familial predisposition
Unknown etiology, possibly autoimmune
Microscopic: The affected areas are devoid of melanocytes

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3
Q

Describe the gross appearance of Melasma.

What other condition(s) is it associated with?

A

Irregular blotchy patches of hyperpigmentation on the face

Associated with oral contraceptive use & pregnancy (“mask of pregnancy”); May regress after pregnancy

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4
Q

What is the common name for Ephelides?
Describe the gross appearance.
What populations are most susceptible?
Describe the microscopic appearance.

A

Freckles!
Light brown macules on face, shoulders, and chest
Common in fair-skinned children - Darken and fade with the season due to sunlight exposure
Microscopic appearance: Increased melanin deposition in the basal cell layer of the epidermis; Normal number of melanocytes

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5
Q

Describe Benign Lentigo.

Describe the microscopic appearance.

A

Benign, localized proliferation of melanocytes that appear
Small, oval, light brown macules
Microscopic appearance shows linear melanocytic hyperplasia
*you are not born with them necessarily (those would be congenital nevi, aka birthmarks)

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6
Q

Congenital (Birthmarks)

A

Present at birth

Giant congenital nevi have increased risk of developing melanoma

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7
Q

Nevocellular Nevus (Mole)
What is the etiology of a nevocellular nevus?
Describe their gross appearance.

A

Benign tumor of melanocytes (melanocytic nevus cells)
Clearly related to sun exposure
Gross appearance: Uniform tan to brown color
Sharp, well circumscribed borders
Tend to be stable in shape and size
Malignant transformation is uncommon

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8
Q

What types of nevi are there?

A

junctional, compound, and intradermal

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9
Q

How do Dysplastic Nevi (BK Moles) differ?

Describe their microscopic appearance.

A

Nevi are larger and irregular and may have pigment variation

Microscopic appearance: the nevus exhibits cytological and architectural atypia

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10
Q

What is Dysplastic Nevus Syndrome?

A

AD (CMM1 gene on chromosome 1)
Often have multiple dysplastic nevi
Increased risk of melanoma

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11
Q

Malignant Melanoma
What is the incidence of malignancy of melanocytes/what is the peak age range?
What are the risk factors?

A

Increasing at a rapid rate; Melanoma peaks in ages 40-70
Risk factors:
Chronic sun exposure, sunburns
Fair-skinned individuals
Dysplastic nevus syndrom
Familial melanoma is associated with loss of function mutation of the p16 tumor suppressor gene on chromosome 9e

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12
Q

What is the gross appearance for malignant melanomas?

Where are the most common locations on the body?

A

Asymmetric, irregular borders, variegated color, large diameter, enlarging, macule, papule, or nodule
Males: upper back
Females: back and legs

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13
Q

What are the different types of malignant melanomas?

A

Lentigo Maligna Melanoma
Superficial Spreading Melanoma
Acral-lentiginous melanoma
nodular melanoma

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14
Q

Where are Lentigo Malignant Melanomas found?

What is the prognosis?

A

Usually located on the face or neck of older individuals

Best prognosis

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15
Q

What is the growth pattern of a superficial spreading melanoma? How commonly does it occur?

A

Has a primarily horizontal growth pattern

Most common type of melanoma

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16
Q

What populations is acral-lentiginous melanoma most common in?
Where is it most commonly found on the body?

A

Most common melanoma in dark-skinned individuals

Affects palms, soles, and subungual area

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17
Q

What is the growth pattern of nodular melanoma?

What is its prognosis?

A

vertical growth pattern

Worst prognosis of the melanoma

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18
Q

What two methods are used to determine the prognosis of malignant melanomas?

A

Staging is by depth of invasion (vertical growth)
Breslow’s thickness
Clark’s levels

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19
Q

What is the Tx for Malignant melanomas

A

Wide surgical excision
Systemic disease is treated with chemotherapy or immunotherapy (interferon)
May even resolve spontaneously

20
Q

Describe Acanthosis Nigricans.
Where is it found?
What co-morbidities is it associated with?

A

Thickened, hyperpigmented skin
Found in the axillae and groin
Often associated with obesity and hyperinsulinism; Associated rarely with internal malignancy (stomach and other gastrointestinal malignancies)

21
Q 
What is Seborrheic Keratosis?
What populations is it common in?
Where is found on the body?
Describe its gross appearance.
Microscopic Appearance.
A

Benign squamoproliferative neoplasm
Very common in middle-aged and elderly individuals
Distribution: trunk, head, neck, and extremities
Gross appearance:
Tan to brown coin-shaped plaques with a granular surface; “stuck on” appearance
Microscopic appearance:
Basaloid epidermal hyperplasia
“Horn cysts” (keratin-filled epidermal pseudocysts)

22
Q

How is Seborrheic Keratosis visually diagnosed?

A

by the “stuck on” appearance, horny pearls or cysts embedded in the structure. Darkly pigmented lesions can be hard to distinguish from nodular melanomas

23
Q

Treatment of Seborrheic Keratosis

A

Usually left untreated; May be removed if they become irritated or for cosmetic purposes

24
Q

What is the Sign of Leser-Trelat (paraneoplastic syndrome)?

A

sudden development of multiple lesions may accompany an underlying malignancy

25
Q

What is Psoriasis?
What is its epidemiology?
What is the most common form?

A

Autoimmune disorder accompanied by increased proliferation and turnover of epidermal keratinocytes
Epidemiology: Affects 1%of the U.S. population
Most common form: psoriasis vulgaris

26
Q

What is the etiology of psoriasis?

A

Unknown etiology
Clear genetic component
May be associate with arthritis, enteropathy, and myopathy

27
Q

What is the gross appearance of Psoriasis?

Where is it commonly located?

A

Gross: the classic skin lesion is a well-demarcated erythematous plaque with a silvery scale
Auspitz sign: removal of scale results in pinpoint bleeding (due to dilated capillaries in the dermis)
Nail beds show pitting and discoloration
Common sites: Knees, elbows, and scalp

28
Q

Pathogenesis of Psoriasis.
Microscopic appearance
What is the treatment?

A

Pathogenesis: increased epidermal turnover
Micro:
Epidermal hyperplasia (Acanthosis)
Patchy Hyperkeratinization with parakeratosis
Uniform elongation and thickening of the rete ridges
Thinning of the epidermis over the dermal papillae
Munro microabscesses
Treatment: Topical steroids and UV irradiation;
Severe systemic disease may be treated with methotrexate

29
Q

What is Pemphigus?

What is the most common form?

A

Rare and potentially fatal autoimmune disorder that is characterized by intra-epidermal blister formation
Pemphigus vulgaris is the most common form

30
Q

What is the Pathogenesis of Pemphigus?

A

production of auto-Abs directed against a part of the keratinocyte desmosome called desmoglein 3 results in loss of intercellular adhesions (acantholysis) and blister formation

31
Q

What are the clinical findings of Pemphigus? Describe its microscopic appearance.

A

Clinical findings: easily ruptured, flaccid blisters are seen classically; Immunofluorescence shows a net-like pattern of IgG staining between the epidermal keratinocytes that create bullae
Microscopic appearance:
Intraepidermal acantholysis; The acantholysis leaves behind a basal layer of keratinocytes, which has a tombstone-like arrangement

32
Q

What is Bullous Pemphigoid?
What is its mechanism?
What are the clinical findings? What does the use of immunofluorescence show?

A

Relatively common autoimmune disorder of older individuals that is characterized by subepidermal blister formation
Production of autoantibodies directed against a part of the keratinocyte hemidesmosome that is called “Bullous Pemphigoid Antigens 1 and 2” results in separation of the epidermis from the dermis and blister formation
Clinical findings: Tense bullae that do not rupture easily; Immunofluorescence shows linear deposits of IgG at the epidermal-dermal junction

33
Q

What is Dermatitis Herpetiformis? What is its mechanism?

A

Rare immune disorder that is often associated with celiac sprue and is characterized by subepidermal blister formation
Production of IgA antibodies directed against gliadin and other antigens that deposit in the tips of the dermal papillae and result in subepidermal blister formation

34
Q

What are the clinical findings of Dermatitis Herpetiformis?
Microscopic Appearance?
Treatment?

A

Clinical Findings: Itchy, grouped vesicles and occasional bullae on the extensor surfaces
Immunofluorescence shows granular IgA deposits at the tips of the dermal papillae
Microscopic Appearance:
Microabscesses are seen at the tips of the dermal papillae
Eventual subepidermal separations results in blister formation
Treatment often responds to a gluten free diet

35
Q

Ichthyosis Vulgaris

A

Common inherited AD skin disorder skin disorder that is characterized by a thickened stratum Corneum with nearly or completely absent stratum Granulosum
Patients have hyperkeratotic, dry skin that particularly involves palms, soles, and extensor areas

36
Q

What does Xerosis cause? Due to what?

A

A common cause of pruritus and dry skin in the elderly that is due to decreased skin lipids

37
Q

Eczema

What is the different between acute and chronic eczema?

A

Group of related inflammatory skin diseases characterized by pruritus
Acute eczema causes a vesicular, erythematous rash
Chronic eczema develops following chronic scratching, and is characterized by dry, thickened hyperkeratotic skin
Atopic dermatitis is due to an IgE-mediated hypersensitivity reaction and causes dry skin and eczem

38
Q

Name two types of contact dermatitis.

A 
Allergic type (poison ivy, nickel in jewelry)
Photodermatitis type (such as photosensitivity reaction after tetracycline)
39
Q

Polymorphous Light Eruption

A

Most common form of photodermatosis and causes erythematous macules, papules, plaques, or vesicles on exposure to sunlight

40
Q

What is Chronic Cutaneous Lupus Erythematous and its mechanism?
What does it cause?

A

Causes epidermal atrophy with deposition of DNA-anti DNA immune complexes in the basement membrane of the epidermis
Causes an erythematous maculopapular eruption that typically involves the nose and cheeks (“butterfly” rash)

41
Q

What is Erythema Multiforme?
What are its main characteristics?
What is the most severe form?

A

A hypersensitivity skin reaction to infections (Mycoplasma pneumonia, herpes simplex) or drugs (sulfonamides, PCN, barbiturates, phenytoin)
EM is characterized by vesicles, bullae, and “targetoid” erythematous lesions
Most severe form is Stevens-Johnson syndrome, which has extensive involvement of skin and mucous membranes

42
Q

Pityriasis Rosea
What infection might precede Pityriasis Rosea?
How big does it appear and where?

A

Causes a pruritic rash that starts with an oval-shaped “herald patch” and progresses to a popular eruption of the trunk that characteristically follows lines of cleavage to produce a “Christmas tree” distribution
An upper respiratory tract infection may precede all other symptoms in as many as 69% of patients
A single, 2- to (rarely) 10-cm oval red “herald” patch appears, classically on the abdomen.
Occasionally, the “herald” patch may occur in a ‘hidden’ position (in the armpit, for example) and not be noticed immediately
It is benign but may inflict substantial discomfort in certain cases

43
Q

What is the classical presentation of Pityriasis Rosea?

What is its etiology?

A

begins with a single “herald patch” lesion, followed in 1 or 2 weeks by a generalized body rash lasting up to 12 weeks (but usually around 6 – 8)
The cause of Pityriasis Rosea is not certain, but its clinical presentation and immunologic reactions suggest a viral infection as a cause

44
Q

Granuloma Annulare
Etiology
Populations

A

Chronic dermatological autoimmune condition which presents as reddish bumps on the skin arranged in a circle or ring
The rings are caused by an autoimmune reaction that causes over-productive leukocytosis
WBCs do not flow freely through blood; instead clump together and can not effectively move through thin capillaries, rising to just underneath the surface of the patient’s skin, resulting in the characteristic rings
It can initially occur at any age and is significantly more common in females (80/20 ratio)
Fairly rare

45
Q

Presentation of Granuloma Annulare.

Associations with other conditions.

A

Causes formation of erythematous papules, which evolve into plaques and involve the back of the hands and feet
It may be associated with diabetes or thyroid disease
It has also been associated with auto-immune diseases such as systemic lupus erythematous, rheumatoid arthritis, and Addison’s disease

46
Q 
Erythema Nodosum
General location on the body?
Associations?
How does it resolve?
Populations?
A

Causes raised, erythematous, painful nodules of subcutaneous adipose tissue
Typically on the anterior shins
Can be associated with granulomatous diseases and strep infection
EN is associated with a wide variety of conditions, including:
Idiopathic
in about 30-50% of cases, the cause of EN is unknown
It can be caused by a variety of conditions, and typically resolves spontaneously within 3–6 weeks
It is common in young people between 12–20 years of age

47
Q

Epidermal Inclusion Cyst

A

A common benign skin cyst lined with stratified squamous epithelium and filled with keratin debris

Pathology 1 (6 decks)

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