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Patho II > The Skin > Flashcards

The Skin Flashcards

1
Q

What are the three layers of the skin?

A

Epidermis
Dermis
Hypodermis

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2
Q

What is the epidermis?

A

Provides a waterproof barrier and creates the skin tone

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3
Q

What is the dermis?

A

Contains tough connective tissue, hair follicles, and sweat glands

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4
Q

What is the hypodermis?

A

Made of fat and connective tissue

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5
Q

What is the stratum corneum of the epidermis made of?

A

Dead keratinocytes

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6
Q

What is the stratum spinosum of the epidermis made of?

A

Dendritic cells

Living Keratinocytes

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7
Q

What is the stratum basale of the epidermis made of?

A

Melanocytes
Dividing Keratinocytes
Tactile cells

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8
Q

What are the primary skin lesions of the skin?

A 
Macule
Patch
Papule
Nodule
Placque
Wheal
Vesicle
Bulla
Pustule
Cyst
Telangiectasia
Tumor
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9
Q

What are secondary skin lesions of the skin?

A 
Scale
Lichenification
Excoriation
Fissure
Erosion
Ulcer
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10
Q

What is a macule?

A

Flat, circumsized area that is a change in color of skin

< 1cm in diameter

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11
Q

What are examples of macules?

A 
Freckles
Flat moles (Nevi)
Petechiae
Measles
Scarlet Fever
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12
Q

What is a patch?

A

Flat, nonpalpable, irregular shaped macule more than 1 cm in diameter

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13
Q

What is an example of a patch?

A

Vitiligo

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14
Q

What is a papule?

A

An elevated, firm, circumsized area

< 1 cm in diameter

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15
Q

What are examples of papules?

A 
Wart
Elevated Moles
Lichen Planus
Fibroma
Insect Bite
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16
Q

What is a nodule?

A

Elevated, firm, circumsized lesion

Deeper in dermis than a papule

1-2 cm in diameter

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17
Q

What is an example of a nodule?

A

Lipomas

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18
Q

What is a placque?

A

Elevated, firm, and rough lesion with flat top surface greater than 1 cm in diameter

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19
Q

What are examples of placques?

A

Psoriasis

Seborrheic and Actinic Keratoses

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20
Q

What is a wheal?

A

Elevated, Irregular shaped area of cutaneous edema

Solid, transient

Variable diameter

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21
Q

What are examples of wheals?

A

Insect bites
Urticaria
Allergic reactions

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22
Q

What is a vesicle?

A

Elevated, circumsized, superficial

Does not extend into dermis

Filled with serous fluid

< 1 cm. in diameter

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23
Q

What are examples of vesicles?

A

Chickenpox
Shingles
Herpes Simplex

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24
Q

What is a bulla?

A

Vesicle more than 1 cm in diameter

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25
Q

What are examples of bulla?

A

Blister

Pemphigus vulgaris

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26
Q

What is a pustule?

A

Elevated, superficial lesions

Similar to a vesicle but with purulent fluid

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27
Q

What are examples of pustules?

A

Impetigo

Acne

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28
Q

What is a cyst?

A

Elevated, circumsized, encapsulated lesion

In dermis or subcutaneous layer

Filled with liquid or semisolid material

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29
Q

What are examples of cysts?

A

Sebaceous cyst

cystic acne

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30
Q

What is Telangiectasia?

A

Fine (0.5-1.0mm), irregular red lines produced by capillary dilation

Can be associated with acne rosacea, venous hypertension, systemic sclerosis, or developmental abnormalities

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31
Q

What is a tumor?

A

Elevated, solid lesion

May be clearly demarcated

Deeper in dermis

More than 2 cm in diameter

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32
Q

What are examples of tumors?

A 
Neoplasms
Benign tumor
Lipoma
Neurofibroma
Hemangioma
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33
Q

What is a scale?

A

Heaped-up, keratinized cells

Flaky skin

Irregular shape

Thick or thin

Dry or oily

Variation in size

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34
Q

What are examples of scale?

A

Flaking of skin with seborrheic dermatitis following scarlet fever

Flaking of skin following a drug reaction

Dry skin

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35
Q

What is Lichenification?

A

Rough, thickened epidermis secondary to persistent rubbing, itching, or skin irritation

Often involves flexor surface of extremity

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36
Q

What is an example of lichenification?

A

Chronic Dermatitis

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37
Q

What is excoriation?

A

Loss of epidermis

Linear, hollowed out, crusted area

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38
Q

What is an example of excoriation?

A

Abrasion or scratch

Scabies

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39
Q

What is a fissure?

A

Linear crack or break form the epidermis to the dermis

May be moist or dry

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40
Q

What are examples of fissures?

A

Athlete’s foot
Cracks in corner of mouth
Anal fissure
dermatitis

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41
Q

What is erosion?

A

Loss of part of the epidermis

Depressed, moist, glistening

Follows rupture of a vesicle or bulla or chemical injury

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42
Q

What is an ulcer?

A

Loss of epidermis and dermis

Concave

Varies in size

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43
Q

What is an example of an ulcer?

A

Pressure ulcer

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44
Q

What is psoriasis?

A

Complex autoimmune inflammatory disease that occurs in genetically susceptible individuals

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45
Q

What is psoriasis characterized by?

A

Well-demarcated erythematous placques with silver scale

46
Q

What are the risk factors for psoriasis?

A

Genetics = PSORS1 locus within MHC on HLA gene and IL-23 related genes

Smoking

Obesity = TNF-alpha

Drugs = beta blockers, lithium, antimalarial

Alcohol

Infections

47
Q

What are patients with psoriasis at a higher risk of getting?

A 
Obesity
Insulin resistance
Metabolic syndrome
Atherosclerosis
Cardiovascular disease
Depression/Stress
48
Q

What occurs in pre-psoriasis skin?

A

1) macrophages, dendritic cells, T cells, many cytokines/chemokines cause the pathological changes in this skin
2) Differentiation of T cells is stimulated by dendritic cells producing IL-23

49
Q

What occurs in Psoriasis skin?

A

1) On exacerbation or onset, activated dendritic cells mainly produce TNFalpha
2) TNF-alpha amplifies inflammation and induces adhesion molecules
3) The clinical success of TNF-blocking agents is therefore not surprising

50
Q

What is Steven Johnson Syndrome/Toxic Epidermal Necrolysis?

A

Severe mucocutaneous reactions most commonly triggered by medications

51
Q

What is SJS/TEN characterized by?

A

Extensive necrosis and detachment of the epidermis

52
Q

What is the difference between SJS and TEN?

A

SJS = desquamation < 10% of body surface

TEN = desquamation > 30% of body surface

53
Q

What are the three theories of pathogenesis of SJS/TEN?

A

1) Medication might upregulate a death receptor mediated apoptotic pathway
2) Drug specific CD8+ cytotoxic T cells release perforin and granzyme B that kill keratinocytes
3) Drug may also trigger the activation of CD8+ T cells, NK cells, and NKT cells to secrete granulysin

54
Q

What is acne vulgaris?

A

Most common cutaneous disorder affecting adolescents and young adults

Disease of Pilosebaceous follicles

55
Q

What are the precursors for clinical lesions of acne vulgaris?

A

Microcomedo

56
Q

What is a closed comedo?

A

Whitehead

Accumulation of sebum and keratinous material formed form a microcomedo

57
Q

What is an open comedo?

A

Blackhead

Folliciular orifice is opened with continued distension

Densely packed keratinocytes, oxidized lipids, adn melanin make the dark color

58
Q

What is caused by follicular rupture in acne vulgaris?

A

Inflammatory papule or nodule

59
Q

What are the four factors involved in acne vulgaris pathogenesis?

A

1) Follicular hyperkeratinization
2) Increased sebum production
3) Propionibacterium acnes within the follicle
4) Inflammation

60
Q

What is Rosacea?

A

Common chronic inflammatory skin with a variety of clinical manifestations primarily localized on the central face

61
Q

What are the four main clinical subtypes of rosacea?

A

Erythematotelangiectatic
Papulopustular
Phymatous
Ocular

62
Q

What are the triggering factors for Rosacea?

A 
UV radiation
Demodex colonization
Microbial Stimuli
heat
Stress
63
Q

What three things are associated with Rosacea pathogenesis?

A

1) Immune dysfunction
2) UV radiation
3) Vascular hyperreactivity

64
Q

What is the immune function pathogenesis of Rosacea?

A

Contributes to the development of chronic inflammation and vascular abnormalities

TLR-2 stimulates release of epidermal proteases and KLK-5

65
Q

What is the pathogenesis of Rosacea from UV radiation

A

UVB radiation induces cutaneous angiogenesis in mice and can stimulate the secretion of VEGF-2 and FGF-2 from keratinocytes

Also stimulates production of ROS

66
Q

What is the pathogenesis of vascular hyperreactivity in Rosacea?

A

Frequent and prolonged flushing is a common feature in rosacea

Triggers of flushing can be spicy foods, alcohol, and extremes of temperature

67
Q

What is melanocytic nevus?

A

Benign proliferations of a type of melanocyte known as a nevus cell

68
Q

What is the difference between melanocytes and nevus cells?

A

melanoctyes are evenly distributed as single units

Nevus cells cluster as nests within lower epidermis and/or dermis

69
Q

What is a junctional nevi?

A

Nests are at the dermalepidermal junction

70
Q

What is a compound nevi?

A

Nests are at the dermalepidermal junction and in the dermis

71
Q

What is an intradermal nevi?

A

Nests are in the dermis

72
Q

What occurs when there is progressive migration of melanoctyes from dermal-epidermial junction into the dermis?

A

Nevi become more elevated and less pigmented

73
Q

What are the predisposing factors of Melanocytic nevi?

A

Heredity
Germline Polymorphisms = IRF4 and TERT
Degress of sun exposure during childhood, especially when intense and sporadic
Phenotypic characteristics such as skin type

74
Q

What are Atypical Acquired Nevi?

A

Benign acquired melanocytic nevi that share, usually to a lesser degree, some of the clinical features of melanoma such as:

Assymmetry
Border Irregularities
Color Variability
Diameter > 6mm

75
Q

Where do Atypical acquired nevi usually appear?

A

On areas of the body that receive sporadic sun exposure

76
Q

What is an eclipse nevus?

A

Type of compound nevus on the scalp of children, a tan center, and brown

Have benign behaviour

77
Q

What is a congenital Melanocytic Nevi (CMN)?

A

Proliferations of benign melanocytes that arise during embryogenesis

78
Q

What is the pathogenesis of CMN?

A

Cellular proliferation via mitogen-activated protein kinase (MAPK)

79
Q

What are the clinical features of CMN?

A

Classically defined as Melanocytic nevi present at birth or within the first few months of life

80
Q

What are complications of CMN?

A

Melanoma can occur after puberty

81
Q

Which phase is it best to catch Melanocytic nevus in?

A

Radial Growth Phase

82
Q

What may stimulate melanocyte proliferation in Melanocytic nevus?

A

FGF released by keratinocytes

83
Q

What is melanoma?

A

Most serious form of cancer

Aggressive neoplasms that may spread in an unpredictable manner to involved virtually any organ in the body

84
Q

How does a melanocyte develop?

A

Modulated by microphthalmia-associated transcription factor (MITF)

MSH stimulated the MC1R

Induction of MC1R activated the expression of MITF causing production of melanin pigments

85
Q

How does tanning cause melanoma?

A

Keratinocyte damage from UV radiation –> p53 mediated induction and POMC expression –> Secretion of MSH and stimulation of MC1R in epidermal malanocytes

86
Q

What is activated in almost all melanomas?

A

MAPK pathway

Growth factor activates in nonmalignant cells but BRAF mutations activate it in invasive melanoma

87
Q

Which melanomas are associated with poorer prognosis?

A

Those with mutations of BRAF

88
Q

What are the ABCDE warning signs of melanoma?

A 
A= assymetry
B = Border
C = Color
D = Diameter 
E = Evolving
89
Q

What is basal cell carcinoma?

A

Common skin cancer arising from basal layer of epidermis

Referrd to as “epithliomas” because of their low metastatic potential

90
Q

What are the risk factors for basal cell carcinoma?

A

Sun exposure
Fair skin, light colored eyes, red hair, northern European ancestry, older age, childhood freckling, and an increased number of past sunburns
Tanning beds
Ionizing radiation

91
Q

What are the two things that contribute to Basal Cell Carcinoma pathogenesis?

A

UV induced inflammation

PTCH1 gene

92
Q

What is the UV induced inflammation of BCC?

A

Clinically results in visible erythema

Prostaglandin synthesis is markedly increased in part through induction of COX2

93
Q

What is the SHH signaling pathway?

A

directs embryonic development of a variety of organs

94
Q

What happens to the PTCH1 gene to cause BCC?

A

PTCH1 has mutations that inactivate it which causes overexpression of the SHH signal

95
Q

What is Cutaneous Squamous Cell Carcinoma (cSCC)?

A

Arising from malignant proliferation of epidermal keratinoctyes

Second most common type of skin cancer in the US

96
Q

What are the risk factors for cSCC?

A

UV light exposure = UVA induced p53 mutations and UVA from tanning beds

Ionizing radiation

Immunosupression

97
Q

What is the hallmark of cSCC?

A

Malignant transformation of epidermal keratinocytes

98
Q

What is the pathophysiology of cSCC?

A

1) Malignant transformation
2) UV induced mutations in p53 gene
3) Mutation in RAS pathway

99
Q

What is impetigo?

A

A contagious superficial bacterial infection observed most frequently in children 2-5 years

100
Q

What are the risk factors for impetigo?

A

Crowding
Poor Hygeine
Underlying Scabies

101
Q

What organisms cause impetigo?

A

S. aureus

Beta-hemolytic streptococci Group A

102
Q

What are the clinical features of impetigo?

A

Non-bullous impetigo
Bullous Impetigo
Ecthyma

103
Q

What is Non-bullous impetigo?

A

Lesions begin as papules that progress to vesicles surrounded by erythema causing rapidly forming crusts with a golden appearance

104
Q

What is bullous impetigo?

A

Strains of S. aureus that produce exfoliative toxin A causing loss of cell adhesion in the epidermis

105
Q

What is Ecthyma?

A

An ulcerative form of impetigo that extends through into the dermis

Consists of “punched out” ulcers covered with yellow crust

106
Q

What is Acanthosis Nigricans?

A

Common condition characterized by velvety, hyperpigmented placques on the neck and axillae

107
Q

What is the clinical significance of Acanthosis Nigricans?

A

Mainly associated with obesity and diabetes mellitus

108
Q

What three types of receptors have abnormalities and cause Acanthosis Nigricans?

A

IGFR1
FGFR
EGFR

109
Q

What is Vitiligo?

A

An aquired pigmentary disorder of unknown origin, is the most frequent cause of depigmentation worldwide

110
Q

What is Vitiligo characterized by?

A

Development of white macules due to the loss of functioning melanocytes in the skin or hair or both

111
Q

What is the Koebner phenomenon?

A

Repeated mechanical trauma (friction) and other types of physical trauma causing vitiligo

112
Q

What is the pathophysiology behind Vitiligo?

A

generation of autoimmune responses against melanocytes

Depigmentation results from hyperactive response of the immune system against melanocytes

Defects of T cell subsets

Increased Autoreactive CD8+ and CD4+ cells

Generation of Anti-melanocyte autoantibodies

Patho II (16 decks)

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