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General and systemic pathology I > 13 - Skin diseases > Flashcards

13 - Skin diseases Flashcards

1
Q

Macule

A

Circumscribed flat skin lesion of differing color than surrounding normal skin

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2
Q

Papule

A

Elevated lesion, often measuring 5 mm or less across

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3
Q

Nodule

A

Elevated solid lesion, often more than 5 mm across

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4
Q

Plaque

A

Mildly elevated lesion with level surface, usually more than 5 mm across

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5
Q

Vesicle

A

Fluid-filled raised lesion measuring 5 mm or less across

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6
Q

Bulla

A

Fluid-filled raised lesion measuring more than 5 mm across; a large vesicle

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7
Q

Circumscribed flat skin lesion of differing color than surrounding normal skin

A

Macule

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8
Q

Elevated lesion, often measuring 5 mm or less across

A

Papule

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9
Q

Elevated solid lesion, often more than 5 mm across

A

Nodule

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10
Q

Mildly elevated lesion with level surface, usually more than 5 mm across

A

Plaque

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11
Q

Fluid-filled raised lesion measuring 5 mm or less across

A

Vesicle

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12
Q

Fluid-filled raised lesion measuring more than 5 mm across; a large vesicle

A

Bulla

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13
Q

Hyperkeratosis

A

Increased thickness of the surface keratin layer

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14
Q

Parakeratosis

A

Pattern of hyperkeratosis characterized by retention of the nuclei

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15
Q

Acanthosis

A

Epidermal hyperplasia = thickening of the spinous epithelial layer

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16
Q

Dyskeratosis

A

Abnormal keratinization occurring prematurely within individual cells or groups of cells below the stratum granulosum

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17
Q

Acantholysis

A

Loss of intercellular connections resulting in loss of cohesion of keratinocytes

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18
Q

Spongiosis

A

Intercellular edema of the epidermis

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19
Q

Acute Eczematous Dermatitis (Eczema)

What are common features of all eczema?

A

Features Common to All Forms of Eczema = Skin Rash

a. Early lesions – red, papular or vesicular, oozing and crusted
b. Persistent (older) lesions – raised, scaling plaques
c. Most rashes are pruritic, but scratching makes them worse

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20
Q

How is acute eczematous dermatitis classified?

A

Contact dermatitis
Cause/Pathogenesis: Topically applied chemicals
Pathogenesis: Delayed hypersensitivity
Clinical features: Marked itching, or burning, or both; requires antecedent exposure

Atopic dermatitis
Cause/Pathogenesis: Unknown; may be heritable
Clinical features: Erythematous plaques in flexural areas; family history of eczema, hay fever or asthma

Drug-related eczematous dermatitis
Cause/Pathogenesis: Systemically administered drug
Example: Penicillin
Pathogenesis: Immediate-type hypersensitivity
Clinical features: Eruption occurs with administration of drug; remits when drug is discontinued

Photoeczematous eruption
Cause/Pathogenesis: Ultraviolet light
Clinical features: Occurs on sun-exposed skin; photo-testing may help in diagnosis

Primary irritant dermatitis
Cause/Pathogenesis: Repeated trauma (rubbing) Clinical features: Localized to site of trauma

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21
Q

What is the treatment for acute eczematous dermatitis?

A

a. Avoid cause of reaction.
b. Protect the skin.
c. Topical corticosteroids will speed healing.

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22
Q

What are initiating factors that may lead to erythema multiforme?

A

a. Infections – commonly herpes simplex
b. Drugs such as penicillin, sulfonamides, barbiturates, salicylates, hydantoins and antimalarials
c. Malignancies – carcinoma and lymphoma
d. Collagen-vascular disease, lupus and polyarteritis nodosa

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23
Q

What are clinical features of erythema multiforme? Sites of involvement?

A

Clinical Features

a. Rapid onset
b. Macules, papules, vesicles and bullae
c. Target lesion –

Sites of Involvement

a. May involve any skin or mucosal surface.
b. Sometimes oral cavity is the only area of involvement.

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24
Q

Etiology of erythema multiforme?

A

Uncommon disorder, acute onset.

It occurs at any age but is more common in childhood to early adulthood.

Exact etiology is unknown, but immune response plays an important role in the cytotoxic reaction that produces lesions.

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25
Q

Treatment of erythema multiforme?

A

Self limiting disorder

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26
Q

What is Stevens-Johnson syndrome?

A

a. This is an extensive and symptomatic febrile form of EM.
b. Skin and mucosal surfaces of mouth, nose, eyes and genitalia are typically involved.
c. Although self-limited, can be life-threatening

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27
Q

What is the etiology and pathogenesis of psoriasis?

A
  • Affects 1-2% of population.
  • The cause of psoriasis is unknown but recent studies suggest there are genetic predisposing factors and autoimmune mechanisms at play.
  • It could be a type of complement-mediated reaction that is localized to the stratum corneum.
  • Occurs at all ages; mean age of onset is 27 years
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28
Q

What are the clinical features, S/S of psoriasis?

A

a. May be associated with arthritis, myopathy, enteropathy and AIDS.
b. Sites – elbows, knees, scalp
c. Typical appearance is a well-demarcated, pink and salmon-colored plaque covered by loosely adherent silver-white scales.
d. Erythroderma – total body erythema and scaling

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29
Q

What histological features/changes are seen in psoriasis?

A

a. Rete ridges are elongated.
b. The granular cell layer is thin or absent, thus dermal papillae are close to the surface.
c. Parakeratosis
d. Munro’s microabscesses –

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30
Q

What are the treatment options for psoriasis?

A

???ADD???

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31
Q

What is the etiology and pathogenesis of lichen planus?

A

Chronic inflammatory disease involves the skin and mucous membranes.

a. Exact etiology is unknown.
b. Recent studies suggest that release of antigens in the basal cell layer and at the dermal-epidermal junction may elicit a cell-mediated cytotoxic immune response.
c. Early studies indicated that there was an association between lichen planus and nervous, worrying type personalities. More recent studies do NOT support this association.

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32
Q

What clinical features does lichen planus present with?

A

a. Presenting signs are the “four Ps” – pruritic, purple, polygonal papules
b. Striae of Wickham –
c. Locations – symmetric distribution particularly on the extremities
d. Oral lesions –

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33
Q

What histopathologic features are found in lichen planus?

A

a. Irregular acanthosis with rete ridges having a “saw tooth” appearance
b. Parakeratosis
c. Liquefactive degeneration of basal cell layer with infiltration of lymphocytes
d. Dense, narrow band of lymphocytes (T cells) in superficial dermis

34
Q

What are the treatment options for lichen planus?

A

a. Skin lesions are usually self-limited and spontaneously resolve after one to two years. Nonetheless, skin lesions often require treatment.
b. Oral lesions tend to persist for years (forever!).
c. If treatment is necessary, topical corticosteroids are used.

35
Q

What is the pathogenesis of pemphigus vulgaris?

A

a. Type II hypersensitivity reaction – antibody dependent cytotoxic reaction
b. IgG antibodies are produced that are directed against proteins of desmosomes, the intercellular cementing substance of epithelial cells of skin and mucous membrane. Autoantibodies targets are:
1. Desmoglein 3
2. Desmoglein 1
c. When autoantibodies bind to antigen, it causes activation of the complement cascade.
d. This causes the epithelial cells to become discohesive, thus vesicles and bullae are formed.

36
Q

What are the clinical features of pemphigus vulgaris?

A

This rare disease is characterized by blistering lesions of the skin and mucous membranes.

a. Both sexes are equally affected.
b. Onset of the disease is usually between 30 and 50 years of age.
c. Any area of skin or mucous membranes may be involved but more common sites are scalp, face, axilla, groin, trunk and points of pressure.
d. Superficial vesicles and bullae rupture easily leaving shallow erosion covered by dried serum and crust.

37
Q

What are the histological features of pemphigus vulgaris?

A

a. Routine staining shows intraepithelial (suprabasal cleft) vesicle and acantholysis.
b. Infiltration of the dermis by lymphocytes, histiocytes and eosinophils is typical.
c. Immunofluorescent studies show lattice-like deposits of IgG and complement in the intercellular areas.

38
Q

What are the treatment options for pemphigus vulgaris?

A

a. This can be a life-threatening disease because of secondary infection and possible dehydration.
b. It cannot be cured but blister formation can be controlled by systemic corticosteroids.

39
Q

What is the pathogenesis in bullous pemphigoid?

A

a. Type II hypersensitivity reaction – antibody dependent cytotoxic reaction
b. IgG autoantibodies are formed against hemidesmosomal antigens in the lamina lucida of the basement membrane of skin and mucosal basement membranes. These are autoantibodies against BP antigens are:
1. Anti-BP230 (BPAg1)
2. Anti-BP180 (BPAg2)
c. Complement activation → dissolution of the basement membrane.
d. The epithelium then detaches from the supporting connective tissue producing a vesicle.

40
Q

What are the clinical features in bullous pemphigoid?

A

a. This disease is generally seen in the elderly.
b. It shows a wide range of clinical presentations.
1. Localized skin involvement only
2. Generalized skin involvement w/wo mucosal involvement
c. Bullae may reach 4 to 8 cm. Bullae are tense and filled with clear fluid.
d. Bullae heal without scarring.
e. Sites of predilection – inner aspect of the thighs, flexor surfaces of the forearms, axilla, groin, and lower abdomen.
f. Oral involvement is seen in up to one third of patients.

41
Q

What are the histological features in bullous pemphigoid?

A

a. Routine staining shows clefting of the epithelium from the dermis at the basement membrane leading to formation of a subepidermal vesicle.
b. Dermis shows infiltration by lymphocytes, some eosinophils and occasional neutrophils.
c. Immunofluorescent stains show linear deposits of IgG and compliment along the basement membrane.

42
Q

What are treatment options for bullous pemphigoid?

A

a. This disease is treated by topical or systemic corticosteroids.
b. Since it is often localized, it does not often lead to life-threatening secondary infections.

43
Q

What is the pathogenesis of mucous membrane pemphigoid?

A

This disease is common in the oral cavity and only rarely involves the skin.
MMP is caused by activity of autoantibodies against basement membrane epitopes and may involve the same autoantibodies as bullous pemphigoid.
Common autoantibody targets are:
1) BP180 (BPAg2)
2) BP230 (BPAg1)
3) Laminin 5
4) Beta 4 integrin

44
Q

What are treatment options for mucous membrane pemphigoid?

A

Usually heals with scarring and is sometimes called cicatricial pemphigoid (cicatrix = scar).

45
Q

What is seborrheic keratosis?

A

Skin lesion of unknown origin and common.
Occur most often in middle-aged or older individuals.
They arise spontaneously and may be numerous.
Locations – trunk, extremities, head and neck
NOT related to skin cancer, BENIGN EPITHELIAL LESION

46
Q

What are the clinical features of seborrheic keratosis?

A

1) Round, flat, coin-like plaques
2) Tan to dark brown
3) Velvety to granular surfaces
4) Size – mm to several cm
5) May peel off but then return

47
Q

What are treatment options?

A

No tx.

Aesthetic tx: liquid nitrogen/laser tx

48
Q

What are verrucae?

A

Warts
Caused by various strains of the human papilloma virus (HPV) which are transmitted by direct contact.
Verruca vulgaris is the common skin wart.
Condyloma accuminata is the venereal wart
Replicates in basal cell layer

49
Q

What are clinical features of verrucae?

A

Lesions are grey-white to tan. They may be flat or convex. The surface is often rough or pebbly.

Sessile elevated skin lesion

  • Normal color to whitish
  • Translucent to opaque
  • Rough surface
  • Cauliflower-like
50
Q

What tx options are there for verrucae?

A

Self limiting, heals spontaneously. May take 6 months-2 years
Cryo, laser, surgical removal

51
Q

What is actinic keratosis?

A

A dysplastic process (premalignant) in the skin.

Has a natural tendency to progress to BCC

52
Q

What is the etiology of actinic keratosis?

A

1) Chronic sun exposure in light pigmented people most commonly
2) Other causes – ionizing radiation, hydrocarbons and arsenic

53
Q

What are clinical features of actinic keratosis?

A

1) Tan brown, red or skin colored lesions, usually less than 1 cm
2) Rough or sandpaper consistency

Macular, plaque or cratered shape
Flesh colored to brown to pink to red
Bigger than seborrheic keratosis

54
Q

What are histologic features of actinic keratosis?

A

1) Hyperkeratosis
2) Epithelial dysplasia of varying degrees, may/may not be present
3) Elastosis of underlying fibrous connective tissue (due to sun exposure, solar elastosis)

55
Q

What treatment options are available for actinic keratosis?

A

Treated by curettage or cryosurgery.
Protection from predisposing factors may help
Can progress to carcinoma over time.

56
Q

What is squamous cell carcinoma? Any sites of predilection?

A

It is the most common cancer arising on sun-exposed sites (skin + mucosa of vermillion lip) of older individuals.
It affects skin and mucosa

57
Q

What are predisposing factors for squamous cell carcinoma?

A

1) Exposure to sunlight and other ionizing radiation
2) Industrial carcinogens – tars and oils
3) Chronic ulcers and draining osteomyelitis
4) Old thermal burn scars
5) Arsenic
6) Immunosuppression

58
Q

What are the clinical features of squamous cell carcinoma?

A

1) Carcinoma-in-situ – sharply defined plaque
2) Invasive stage
a) May be flat, nodular or cratered.
b) Red scaly surface
c) May ulcerate and bleed.
d) Margins often indurated

59
Q

What are the histologic features of squamous cell carcinoma?

A

1) Nests, strands and individual cells invade the dermis.
2) Keratin pearls and dyskeratotic cells may be present.
3) Differentiation
a) Well differentiated
b) Moderately differentiated
c) Poorly differentiated

60
Q

Behavior and treatment options for squamous cell carcinoma

A

1) Usually are identified and treated while small.
2) Less than 5% have metastasis to regional lymph nodes at the time of diagnosis.
3) Treated by excision, sometimes by radiation.

Lip is most curable. > 90% cure rate
Prognosis depends on stage and site

61
Q

What is basal cell carcinoma?

A

It is a slowly growing skin tumor that rarely metastasizes. Basal cell carcinoma is the most common malignant skin tumor.
It does NOT affect the mucosa but is INVASIVE.

62
Q

What are predisposing factors or basal cell carcinoma? Are there any sites of predilection?

A

1) Fair skin
2) Sun exposure
3) Immunosuppression
4) Nevoid basal cell carcinoma syndrome –
-Autosomal dominant Mendelian disorder
-Multiple basal cell carcinoma
-Multiple odontogenic keratocysts
-Bifid ribs and other rib malformations
-Can get BCC in teens
Middle + upper face: cheeks, nose, temple, forehead

63
Q

What are clinical features of basal cell carcinoma?

A

1) Flat or plaque-like, but may be nodular.
2) Surface may be smooth or crusty.
3) May ulcerate and bleed, or mimic non-healing pimple.
4) Size –
5) Often multiple

  1. Central crater common, w/ rolled edge/border
64
Q

What is the behavior and prognosis of basal cell carcinoma?

A

1) This is one of the most indolent malignant tumors.
2) It is usually cured by local excision.
3) Although it rarely metastasizes, it may become very large and locally destructive if not treated. Can be lethal.

  1. Invasive
65
Q

What is vitiligo? What are clinical features of vitiligo? Etiology?

A
  1. This disease features well-demarcated areas of pigment loss.
  2. It is caused by complete or partial loss of pigment-producing melanocytes within the epidermis.
  3. It is a common disorder that affects all races but is more noticeable in darkly pigmented people.

Idiopathic - may be familial
Must R/O infection, autoimmune ds, etc., make sure it is not secondary to something else.

66
Q

What are ephilides? (ephelis)

A

Freckles.
1. Ephilides are the most common pigmented lesions of childhood.

  1. Freckles are predominantly seen in Caucasians.
67
Q

What is the etiology of ephilides?

A

Hyperpigmentation follows sun exposure and is due to increased amounts of melanin pigment within basal keratinocytes.

68
Q

What are the clinical features of ephilides? Histological?

A

Clinical:
Small flat tan to brown macules. Always flat, symmetric, small.
Usually multiple and numerous.
More common on face, can be anywhere

Histo:
Normal # and distribution of melanocytes
Excess production of melanin.

69
Q

What is a melanocytic nevus? (pigmented nevus)

A

A mole.

Tumor-like lesions are congenital or acquired hamartomas of melanocytes.

70
Q

What are the clinical features of a melanocytic nevus?

A

a. Well-defined flat or elevated lesion
b. Uniformly pigmented, tan to brown
c. Small – usually < 1 cm
d. Most develop during childhood or early adulthood.

Round, oval.

71
Q

What are the histological features of a melanocytic nevus?

A

a. Junctional nevus – round to oval nevus cells grow along dermal-epidermal junction and contain varying amounts of melanin pigment.
b. Compound nevus – nests of pigmented nevus cells are present in the upper dermis and at the dermal-epidermal junction. (Both dermal and junctional).
c. Dermal (intradermal) nevus – nests of pigmented nevus cells are present in the upper dermis only.

72
Q

Are there any treatment options for a melanocytic nevus?

A

Usually, no treatment. Only for esthetics.
Removal can cause scarring!
Be suspicious of moles developing in ADULTHOOD! May be MALIGNANT MELANOMA!

73
Q

What is a dysplastic nevi?

A
  1. Until recently, the dysplastic nevus was considered to be a distinct histologic form of nevocellular nevus and was thought to be a precursor of malignant melanoma.
  2. It is now recognized that dysplastic nevus is NOT a histologic diagnosis. A more appropriate usage of the term is as “Dysplastic Nevus Syndrome,” a diagnosis of which can be made only on the basis of clinical findings.
74
Q

What are the clinical features of a dysplastic nevi?

A

a. Multiple, possibly hundreds, of nevi which may be larger than other acquired nevi.
b. Nevi may be flat or slightly raised.
c. Nevi usually show variation in pigmentation.
d. Nevi often show borders that are irregular in contour.
e. Nevi may occur on sun-exposed or non-sun-exposed surfaces.
f. Often seen in persons with family history of dysplastic nevus syndrome

75
Q

What kind of behavior do dysplastic nevi exhibit?

A

a. Due to the sheer numbers of pigmented nevi, there is a risk of malignant transformation to malignant melanoma for any given nevus.
b. Patients with the syndrome need careful monitoring by a dermatologist to provide early diagnosis and treatment of a melanoma, should it arise.

76
Q

What is a malignant melanoma? (melanoma)

A

A malignant neoplasm of melanocytes. It may or may not actually be pigmented

77
Q

What risk factors are associated with melanoma?

A

1) Exposure to sunlight, especially during infancy and childhood
a) Men – upper back
b) Women – back and legs
2) Light normal pigmentation
3) Other factors include dysplastic nevus syndrome, hereditary factors and exposure to carcinogens.

78
Q

What are clinical warning signs of melanoma?

A

a. A – Asymmetry
b. B – Border that is irregular or notched
c. C – Color that is variegated
d. D – Diameter that is greater than 6 mm or the diameter of a pencil eraser
e. E – Evolution of lesion, i.e., there has been change in an existing pigmented lesion

79
Q

What are histologic features of melanoma?

A

a. Nevus cells may proliferate in nests or solid sheets.
b. Individual cells are enlarged and often bizarre.
c. Histologic Growth Patterns
1) Radial growth phase – the melanoma has a tendency to grow horizontally within the epidermal and superficial dermal layers. This stage may last for a prolonged period of time. Melanoma does NOT have the capacity to metastasize in this stage.
2) Vertical growth phase – the melanoma now grows downward into the deeper dermal layers as an expansile mass. Clinically, the melanoma develops a nodule within the previously flat lesion. This stage features metastatic potential

80
Q

What are the available treatment options for melanoma? How is the prognosis?

A

Tx:

a. Complete surgical excision.
b. Depending on depth of invasion at the primary site, local lymph nodes may also be surgically removed.

Prognosis:

a. In 1945 the 5-year survival rate was about 40%.
b. In 1983 the 5-year survival rate was 83%.
c. Factors that affect prognosis
1) Early detection and treatment in the lateral growth phase (< 2 cm diameter). 5-year disease-free survival is 100%.
2) Tumor thickness and presence (or absence) of ulceration have prognostic significance independent of clinical stage.
3) Depth of invasion in the vertical growth phase
4) < 0.76 mm invasion yields best survival → 5-year disease-free survival 98%
5) < 1.7 mm tumor thickness is still considered favorable.

General and systemic pathology I (13 decks)

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