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Pathophysiology > Dermatology > Flashcards

Dermatology Flashcards

1
Q

Describe excoriation.

Macroscopic

A

Traumatic lesions breaking the epidermis, causing linear area (scratches)

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2
Q

Define lichenification.

Macroscopic

A

Thickened, red, rough skin; excessive scratching/rubbing

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3
Q

Define macule and patch.

Macroscopic

A

Circumscribed, FLAT lesion distinguished by surrounding skin color

Macule < 5 mm < Patch

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4
Q

Define onycholysis.

Macroscopic

A

Separation of nail plate from nail bed.

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5
Q

Define papule and nodule.

Macroscopic

A

Elevated, DOME-SHAPED lesion.

Papules < 5 mm < Nodule

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6
Q

Define plaque.

Macroscopic

A

Elevated, FLAT-TOPPED lesion

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7
Q

Define pustule.

Macroscopic

A

Discrete, PUS-FILLED, raised lesion.

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8
Q

Define scale.

Macroscopic

A

Dry, horny, PLATE-LIKE excrescence; imperfect cornification.

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9
Q

Define vesicle and bulla.

Macroscopic

A

Fluid-filled, raised lesion.

Vesicle < 5 mm < Bulla

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10
Q

Define wheal.

Macroscopic

A

Itchy, transient, elevated lesion with variable blanching and erythema formed from dermal edema.

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11
Q

Define acanthosis.

Microscopic

A

Diffuse epidermal hyperplasia. (Psoriasis)

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12
Q

Define dyskeratosis.

Microscopic

A

Abnormal, premature keratinization within cells below the s. granulosum.

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13
Q

Define erosion.

Microscopic

A

Discontinuity of skin showing incomplete loss of epidermis.

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14
Q

Define exocytosis.

Microscopic

A

Infiltration of epidermis by inflammatory cells.

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15
Q

Define hydropic swelling (ballooning).

Microscopic

A

Intracellular edema of keratinocytes, seen in viral infections.

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16
Q

Define hypergranulosis.

Microscopic

A

Hyperplasia of s. granulosum; d/t intense rubbing

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17
Q

Define hyperkeratosis.

Microscopic

A

Thickening of the s. corneum; qualitative abnormality of keratin.

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18
Q

Define lentinginous.

Microscopic

A

Linear pattern of melanocyte proliferation w/i epidermal basal cell layer.

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19
Q

Define papillomatosis.

Microscopic

A

Surface elevation caused by hyperplasia and enlargement of contiguous dermal papillae.

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20
Q

Define parakeratosis.

Microscopic

A

Keratinization with retained nuclei in s. corneum.

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21
Q

Define spongiosis.

Microscopic

A

INTERcellular edema of the epidermis.

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22
Q

Define ulceration.

A

Discontinuity of skin showing complete loss of epidermis, reveals dermis and subcutis

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23
Q

Define vacuolization.

A

Formation of vacuoles within or adjacent cells; basal cell-basement membrane zone area

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24
Q

What is the most common type of nevi and how the presence of nevi is correlated with potential increased risk of melanoma?

A

Most common:
Acquired melanocytic nevi (junctional, compound, intradermal)

Congenital and dysplastic nevi carry increased risk of melanoma.

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25
Q

What are the genetic and causative agents of melanoma?

A

Linked to mutations caused by UV radiation exposure to sunlight. Can be inherited as autosomal dominant.

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26
Q

What are the potential precursor to melanoma?

A

Dysplastic nevi can progress to melanoma but melanoma can also arise spontaneously.

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27
Q

Describe the range of morphologic findings of melanoma.

A

Striking variations in color; borders are notched/irregular.

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28
Q

What are the ABCDE’s of melanoma?

A 
Asymmetry.
Border, irregular.
Color, variegated
Diameter, increasing.
Evolving
29
Q

Describe epidemiology, locations and clinical findings of seborrheic keratoses.

A

Epidemiology - middle-aged adults; spontaneous

Location: trunk, head, neck, extremities

Clinical findings: round, flat coin-like waxy plaque; tan to dark brown; velvety

30
Q

Describe appearance of acanthosis nigricans.

A

Thickened, hyperpigmented skin with “velvet-like” texture usually in flexural areas.

31
Q

What common conditions are associated with acanthosis nigricans?

A

Diabetes mellitus, obesity, GI adenocarcinoma.

32
Q

What is the etiologic agent or inciting event in the development of actinic keratoses?

A

Sun damage!

33
Q

What are the risks and incidences of malignant transformation of actinic keratoses?

A

Risk of progression to small cell carcinoma. True risk of progression is unknown.

34
Q

What are the common clinical features of actinic keratoses?

A

< 1 cm.

Tan-brown, red, rough, sandpaper consistency.

35
Q

Identify the causative agent(s) and/or exposure(s) of squamous cell carcinoma.

A

Cumulative UV damage from sunlight, chronic ulcers, HPV 5 and 8, tobacco

36
Q

What is the risk of squamous cell carcinoma metastasis and the clinical morphologic features of the lesion?

A

Risk - very low (~5%)

Features:
In situ - sharply defined, red, scaling plaques
Advanced = nodular, hyperkeratotic scale, may ulcerate

37
Q

Identify the causative agent(s) and/or exposure(s) of basal cell carcinoma.

A

Sun exposure; immunosuppression, disorders in DNA repair.

38
Q

What is the risk of basal cell carcinoma metastasis and the clinical morphologic features of the lesion?

A

Risk - very, very low

Features: pearly papules with telangiectasias, may resemble melanocytic nevi

39
Q

What is urticaria, its characteristics, and its underlying mechanism of injury?

A

Hives; small, pruritic edematous plaque (wheal).

Mast cell degranulation with resulting vascular permeability, IgE mediated.

40
Q

Define angioedema.

A

Edema extending to the deeper dermis and subcutaneous layers.

41
Q

List the 5 categories of eczematous dermatitis.

A
  1. Allergic contact
  2. Atopic
  3. Drug-related
  4. Photoeczematous
  5. Primary Irritant
42
Q

What is the pathogenesis and gross morphologic change of eczematous dermatitis?

A

Pathogenesis: T-cell mediated Type IV hypersentivity

Morphology: pruritic, red, paulovesicular, oozing, crusted lesions. develop reactive acanthosis and hyperkeratosis producing scales

43
Q

What are the 4 main general categories of conditions associated with erythema multiforme?

A
  1. Infections
  2. Drug exposure
  3. Cancer
  4. Collagen vascular disease
44
Q

What is the pathogenesis of erythema multiforme?

A

Keratinocyte injury mediated by skin-homing CD8+CTLs.

45
Q

What are the clinical findings of erythema multiforme?

A

Diverse lesions; macules, papules, vesicles, targetoid lesions

46
Q

What are the clinical findings of Stevens-Johnson Syndrome?

A

Fever and lesions of lips/oral mucosa, conjunctiva, urethra, genitals. Loss of skin integrity and infections leading to life-threatening sepsis

47
Q

What are the clinical findings of toxic epidermal necrolysis?

A

Diffuse necrosis and sloughing of cutaneous and mucosal epithelial surfaces; similar to patients with extensive burns

48
Q

Define psoriasis and the correlating HLA genes.

A

Chronic inflammatory dermatosis; HLA-C positivity shows strong correlation.

49
Q

What are the common anatomical sites affected by psoriasis? What are the gross appearances?

A

Sites: skin of elbows, knees, scalp, lumbosacral areas, glans penis, pitting in nail bed.

Appearance: well demarcated, pink to salmon-colored plaque covered by silver-white scale

50
Q

Psoriasis is a common cause of…

A

Inflammatory arthritis

51
Q

Describe the characteristic locations and lesions of seborrheic dermatitis.

A

Location: high density sebaceous glands - scalp, forehead, external auditory canal, nasolabial folds, presternal area

Lesions: macules and papules on erythematous-yellow greasy base; scaling and crusting

52
Q

What are the 6 “P”s of lichen planus?

A
  1. Pruritic
  2. Purple
  3. Polygonal
  4. Planar
  5. Papules
  6. Plaques
53
Q

What are the common clinical features of lichen planus?

A

Itchy, flat-topped papules with white dots/lines (Wickham striae); symmetrically distributed; extremities, wrists, elbows, glans penis

Oral lesions - white, reticulated, netlike areas

54
Q

Describe the “typical” patient with pemphigus.

A

40s - 60s

Men, women equally affected

55
Q

Describe the lesions associated with pemphigus vulgaris.

A

Superficial vesicles and bullae that rupture easily leaving shallow erosions covered with dried serum and crust.

56
Q

Describe the findings of bullous pemphigoid.

A

Tense bullae fille with clear fluid; erythematous; < usually 2 cm in diameter, does not rupture easily, heal w/o scarring

57
Q

Describe the “typical” patient with acne vulgaris.

A

Mid to late teens; boys > girls

58
Q

What situations may induce or exacerbate acne vulgaris?

A

Drugs, occupational exposures, occlusion of sebaceous glands

59
Q

What are the clinical findings of open and closed comedones?

A

Open: small follicular papules containing black keratin plug (blackheads)

Closed: follicular papules without visible central plug (whiteheads)

60
Q

Describe a “typical” patient with rosacea.

A

Middle age and up, female > male

61
Q

What are the four stages of rosacea disease process?

A
  1. Flushing episodes
  2. Persistent ertyema and telangiectasia
  3. Pustules and papules
  4. Rhinophyma, thickening of nasal skin w/ erythematous papules and prominent follicles.
62
Q

Define panniculitis.

A

Inflammatory reaction in the subcutaneous adipose tissue affecting the fat lobules and/or connective tissues that separates the fat into lobules

63
Q

What are the clinical signs and symptoms of erythema nodosum?

A

Poorly defined, tender, erythematous plaques and nodules; fever and malaise

64
Q

What are the categories of clinical conditions associated with panniculitis?

A

Infections, drug administration, sarcoodisosis, IBS, malignant neoplasm.

65
Q

What is the etiologic agent of verrucae and its route of transmission?

A

HPV, direct contact or autoinoculation

66
Q

Describe the lesions of verruca vulgaris.

A

On dorsal hands, gray-white to tan, flat to convex, rough pebble-like surface

67
Q

What is etiologic agent of molluscum contagiosum and its route of transmission?

A

Pox virus via direct contact

68
Q

Describe the typical lesions and delineate where they are most commonly found.

A

Firm, pruritic, pink to skin-colored umbilicated papules; 0.2 - 0.4 cm.

Multiple lesions on skin, mucous membranes, trunk and anogenital areas.

Pathophysiology (9 decks)

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