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Pathology Pt. 5 > Skin > Flashcards

Skin Flashcards

1
Q

What characteristics are shared by all forms of eczema?

A

Early stage lesions are red, papulovesicular, oozing, and crusted. Late lesions develop into raised, scaling plaques.

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2
Q

What are the five forms of acute eczematous dermatitis?

A
  1. Allergic contact
  2. Atopic - defects in keratinocyte barrier function.
  3. Drug-related
  4. Photo-eczematous
  5. Primary irritant
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3
Q

Do most forms of eczema resolve upon removal of the stimulus?

A

Yeah

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4
Q

What morphological change is characteristic of acute eczematous dermatitis? Describe it.

A

Spongiosis: accumulation of edema between keratinocytes –> breaking of desmosomes. There is also lymphocytic infiltrate, mast cell degranulation, and eosinophil infiltrate (eosinophils are mostly seen in drug-induced type)

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5
Q

Allergic contact dermatitis is a type ____ hypersensitivity reaction in which ____ cells migrate to the affected area, and release cytokines to attract more inflammatory cells.

A

type 4, T cells

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6
Q

What are the clinical features of acute eczematous dermatitis (2)?

A
  1. Lesions are pruritic (itchy), edematous, and oozing, often containing vesicles and bullae.
  2. Persistent stimulation –> scaly lesions (hyperkeratosis), epidermis thickens (acanthosis)
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7
Q

Describe the stages of eczema development.

A
  1. Initial dermal edema and perivascular infiltration by inflammatory cells.
  2. 24-48 hours - epidermal spongiosis and microvesicle formation.
  3. Persistent stimulation leads to parakeratosis (thickened stratum corneum with retained nuclei), acanthosis, and hyperkeratosis.
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8
Q

Psoriasis is a chronic inflammatory skin disease characterized by _________ __________.

A

epidermal hyperplasia

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9
Q

Is psoriasis familial? How common is it? At what age does it usually manifest?

A

Yeah familial (1/3 have family Hx, 65% monozygotic twin concordance). It affects 1-2% of the worldwide population. Can arise at any age but usually does in late adolescence.

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10
Q

Psoriasis is associated with increased risk of _____ _______, ________, and ______.

A

heart attack, strokes and arthritis

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11
Q

True or false: the pathogenesis of psoriasis is poorly understood and likely multifactorial.

A

True

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12
Q

It is thought that _________ of epidermal proliferation and an abnormality in the ________ ________ produce psoriatic lesions.

A

deregulation of epidermal proliferation and an abnormality in the dermal microcirculation

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13
Q

Describe the microcirculatory changes that are seen in psoriasis (2).

A
  1. Capillary loops of dermal papillae become venular, showing multiple layers of basal lamina material.
  2. Lots of neutrophils at the tips of dermal papillae, and they migrate into the epidermis and stratum corneum.
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14
Q

What areas of the body are most often affected by psoriasis (6)?

A

Elbows, knees, scalp, lumbosacral areas, intergluteal cleft, glans penis

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15
Q

Describe the gross appearance of a typical psoriatic lesion (2).

A
  1. Well-demarcated pink or salmon colored plaque

2. Covered by loosely adherent scale that is silver-white

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16
Q

Nail changes occur in ___% of cases of psoriasis. Describe these changes (5).

A

30%

  1. Yellow-brown color
  2. Pitting
  3. Dimpling
  4. Separation of the nail plate from the underlying bed
  5. Thickening and crumbling
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17
Q

Describe the microscopic changes seen in a psoriatic lesion. (5)

A
  1. Increased cell turnover –> epidermal thickening (acanthosis) with regular downward elongation of the rete bridges.
  2. Mitotic figures seen ABOVE the basal layer.
  3. Thinned or absent stratum granulosum.
  4. Extensive overlying parakeratotic scale.
  5. Neutrophils form small aggregates with spongiotic foci in the epidermis and stratum corneum.

Easier: acanthosis, parakeratosis, neutrophils everywhere, mitotic figures above the basal layer, thin or absent stratum granulosum.

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18
Q

What happens when you scrape off the scale of a psoriatic lesion?

A

Auspitz sign - multiple minute bleeding points

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19
Q

What is verrucae (warts) and what causes them?

A

Cutaneous tumors caused by low-risk HPV (no transforming potential)

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20
Q

How do warts spread?

A

Direct contact - can be autoinoculation, too

21
Q

Do verrucae spontaneously regress?

A

Usually within 6 months to 2 years

22
Q

Describe how HPV causes warts.

A

It subverts cell cycle control to allow for increased proliferation and survival of epithelial cells and new virus production. Normal immune response limits growth. If immunocompromised –> high numbers, large wart sizes.

23
Q

Describe the microscopic morphological changes seen in verrucae (4).

A
  1. Epidermal hyperplasia that is UNDULANT (wave-like).
  2. Koilocytosis - cytoplasmic vacuolization (perinuclear halo).
  3. Prominent keratohyaline granules.
  4. Jagged eosinophilic intracytoplasmic protein aggregates.
24
Q

What are the two types of verrucae?

A

verruca vulgaris (common wart), verruca plana (plantaris and palmaris are subtypes)

25
Q

Describe ten changes seen in a common wart (verruca vulgaris). What HPV types is it associated with?

A
  1. Elevated papule with a verrucous, rough, pebble-like surface.
  2. Single or multiple.
  3. Often found on dorsal surfaces of hands or on the face.
  4. Gray-white or tan.
  5. Flat or convex.
  6. 0.1-1 cm
  7. Hyperkeratosis
  8. Papillary epidermal hyperplasia and koilocytes.
  9. Radiate symmetry.
  10. Prominent keratohyalin granules.

HPV 2, 4, no malignant potential

26
Q

Describe the morphological changes seen in verruca plana (flat warts). What HPV types cause it?

A

Rough, scaly lesions, 1-2 cm, can be confused with calluses. They grow inwards, and are found on the palm or soles of the feet.

HPV 3, 10 cause it

27
Q

What is actinic keratosis?

A

A premalignant epithelial lesion with dysplasia.

28
Q

Describe the microscopic morphologic changes seen in actinic keratosis (4).

A
  1. Thickened dermis (hyperkeratosis).
  2. Blue-gray elastic fibers (solar elastosis) from chronic sun damage.
  3. Stratum corneum is thickened with retained nuclei (parakeratosis).
  4. Lower portions of the epidermis show atypia with hyperplasia of basal cells.
29
Q

What causes actinic keratosis? Can it become malignant?

A

Sun damage –> UV p53 damage. They can progress to carcinoma in situ.

30
Q

Describe the gross changes seen in actinic keratosis (4).

A
  1. Usually less than 1 cm diameter
  2. Tan-brown, red, or skin colored
  3. Rough, sandpaper-like
  4. Happens on sun-exposed areas
31
Q

How should actinic keratosis be treated?

A

WIth cryotherapy or topical chemo agents

32
Q

What causes squamous cell carcinomas?

A

UV exposure –> DNA damage goes unrepaired

33
Q

In squamous cell carcinoma, mutations in _____ and _____ are common. They are also common in immunosuppressed individuals or individuals with _________ _________.

A

p53, RAS mutations are common

xeroderma pigmentosum

34
Q

Describe the microscopic changes seen in squamous cell carcinomas (6).

A
  1. Highly atypical cells at all epidermal levels with nuclear crowding and disorganization.
  2. Dysplasia is broad and occupies the full thickness of the epithelium.
  3. Once they break through the BM –> invasive
  4. Invasive carcinomas have variable differentiation
  5. All squamous cell carcinomas share the feature of keratinization (KERATIN PEARLS) - especially well-differentiated ones.
  6. Enlarged nuclei, prominent nucleoli.
35
Q

Describe the gross changes seen in a squamous cell carcinoma (2).

A
  1. Sharply defined scaling plaque; can arise from actinic keratosis.
  2. Advanced, invasive lesions are nodular, show variable scale and may ulcerate.
36
Q

The likelihood of metastasis of a squamous cell carcinoma is related to the __________ of the lesion and the ________ of ________ into the subcutis

A

related to the thickness of the lesion and the degree of invasion into the subcutis

37
Q

What percentage of cases of squamous cell carcinoma have metastasized to regional nodes at the time of diagnosis? How are they treated?

A

Only 5% have metastasized. They are often found when small and resectable. Treatments are electrocautery, topical chemo, excision, or radiation.

38
Q

Are melanomas common? Are they more dangerous?

A

Less common but more deadly than basal or squamous cell carcinoma

39
Q

Where do melanomas arise on the body?

A

Mostly on skin but can also arise on oral and genital mucosal surfaces, esophagus, meninges, and in the eyes.

40
Q

What is the biggest risk factor in the development of a melanoma?

A

Sun exposure

41
Q

Melanomas are more likely to occur in _____-skinned people and in places with high sun exposure. Risk is also related to sun exposure in early life, especially involving ________ _________. Hereditary predisposition also plays a role.

A

fair-skinned people

early blistering sunburns - bad

42
Q

Malignant transformation of melanocytes is a _______ process involving activating mutations in proto-oncogenes and loss of function mutations in tumor suppressor genes.

A

multistep

43
Q

What is the most important factor in prognosticating a melanoma? What are seven other factors?

A

Depth of invasion - most important.

  1. Lymphatic density
  2. Mitotic rate
  3. Overlying ulceration
  4. Evidence of regression
  5. Presence of infiltrating lymphocytes (more is better)
  6. Gender (female is better)
  7. Location (extremities are better)
44
Q

Describe the growth phases of a melanoma.

A

Radial growth phase: it grows horizontally within the epidermis and superficial dermal layers for a while. Melanocytes grow singly within the epidermis at all levels but as large irregular-sized nests at the dermal-epidermal junction.

Vertical growth phase: downward invasion - happens unpredictably.

45
Q

How does a melanoma metastasize?

A

To regional lymph nodes. Can also spread hematogenously to anywhere (lungs, brain, liver)

46
Q

What is the most important clinical sign of a melanoma?

A

The change in color or size of a pigmented lesion

47
Q

Name six warning signs of a melanoma.

A
  1. Enlargement of a preexisting mole
  2. Itching or pain in a preexisting mole
  3. Development of a new pigmented lesion in adulthood
  4. Irregular borders of a pigmented lesion
  5. Color changing in a pigmented lesion
  6. ABCs: assymetry, border, color, diameter, evolution
48
Q

How are melanomas most often treated? What is the prognosis for those that have metastasized?

A

Treated surgically or with drugs that turn off endogenous immune inhibitors. Melanoma vaccines - using tumor antigens to mount immune response.

Metastasis –> poor prognosis

Pathology Pt. 5 (7 decks)

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