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Clinical Medicine > Dermatology Lecture 1 > Flashcards

Dermatology Lecture 1 Flashcards

1
Q

3 main layers of skin

A

Epidermis - barrier from environment, waterproof
Dermis - vessels, glands, hair follicles, nails, nerves
Hypodermis - subcutaneous fat and connective tissue

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2
Q

List the layers of the epidermis from superficial to deep

A 
Stratum corneum
Stratum lucidum
Stratum Granulosum
Stratum spinosum
Stratum basale
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3
Q

Feature of stratum corneum?

A

superficial layer with shedding dead skin

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4
Q

Feature of stratum lucidum?

A

found on palmar and plantar surfaces

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5
Q

Feature of stratum granulosum?

A

keratinization

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6
Q

Feature of stratum spinosum?

A

spiny-shaped cells (strength and flexibility)

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7
Q

Feature of stratum basale

A

Cells germinate - keratinocytes

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8
Q

Types of cells within epidermis

A

keratinocytes, melanocytes, merkel cells, langerhans cells

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9
Q

Features of keratinocytes
Is it common?
What is the deeper layer called?

A

most common cell in epidermis

forms a barrier and in the deeper layer, they are called basal cells

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10
Q

Features of langerhan’s cells
What are they derived from?
What is their function?
What percentage of epidermal cells are langerhan’s cells?

A

dendritic cells scattered throughout epidermis (5% of epidermal cells)
Derived from bone marrow
Have immunologic function - “serve as macrophages of skin” by presenting antigens to lymphocytes

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11
Q

What cells are the macrophages of the skin and have an immunologic function?

A

Langerhan’s cells

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12
Q

Merkel Cells
What do they do?
Where do they exist?
Special function?

A

Mechanoreceptors for light touch; abundant on fingertips

May have a neuroendocrine function

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13
Q

Which cells may have neuroendocrine function?

A

Merkel cells in epidermis

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14
Q

Melanocytes
- what do they protect against?
Without melanin, what are people more likely to develop?
More melanin has what effect on skin tone?
Does more melanin make it more or less difficult to synthesize Vit D?
What is melanin synthesized from and how is it packaged?

A

protects against UV radiation
without melanin, more susceptible to development of skin cancer
more melanin = darker skin tone
more melanin = more difficult to synthesize Vit D
Melanin is synthesized from tyrosine and packaged in melanosomes

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15
Q

What is the dermis?

A

Support structure that contains blood, lymph vessels, nerves, hair follicles, glands, and fibrous tissue

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16
Q

Layers of dermis?

A

Papillary dermis - superficial
Reticular dermis - deep
Ground substance

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17
Q

Papillary dermis contains

A

loose network of fine collagen

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18
Q

Reticular dermis contains

A

densely packed and thick collagen bundles; elastic fibers are largely located here

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19
Q

Ground substance contains

A

proteoglycans and glycosaminoglycans

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20
Q

Basement membrane zone

A

dermal-epidermal junction and barrier for malignant cells

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21
Q

Two layers of basement membrane zone

A

Basal lamina and reticular connective tissue

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22
Q

Basal lamina layers

A

Lamina lucida and lamina densa

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23
Q

Describe lamina lucida.

A

clear zone traversed by transmembranous proteins

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24
Q

Describe lamina densa.

A

dense zone of type IV collagen derived from epidermal cells

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25
Q

Describe reticular connective tissue.

A

thick fibrous bands of type VII collagen connecting into dermis; anchoring fibrils

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26
Q

Defects in the Basement membrane zone are the basis for what type of diseases?

A

blistering

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27
Q

Hypodermis contains

A

fibroblasts, adipose, and macrophages
subcutaneous fat
larger vessels and nerves

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28
Q

Describe subcutaneous fat of hypodermis.

A

Deepest layer. network of collagen and fat cells. conserves heat and provides shock absorbency

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29
Q

What layer conserves heat and provides shock absorbency?

A

Subcutaneous fat of hypodermis layer

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30
Q

Eccrine gland function

A

Temperature regulation

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31
Q

What type of gland is eccrine gland and where is it located? What is its function?

A

Coiled gland in deep dermis for secretion

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32
Q

Straight duct extends to _______ to transport sweat to surface of skin

A

epidermis

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33
Q

Eccrine covers ____ of the body and releases at ____ of skin.

A

most, surface

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34
Q

How many eccrine glands are there? What is secretory capacity?

A

2-3 million

10 L/day secretory capacity

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35
Q

Eccrine - Sweat begins as _______ with plasma, however due to _______ reabsorption in duct, becomes ______

A

isotonic, electrolyte, hypotonic

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36
Q

Apocine glands secrete into ______

A

sac of hair follicles

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37
Q

Apocrine are concentrated in what two regions? Where are modified glands located?

A

Axillary and anogenital regions; modified glands in eyelids, breasts, ears

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38
Q

Apocrine glands release what kind of fluid?

A

thick, clear, odorless

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39
Q

Why does body odor occur?

A

bacteria acts upon apocrine secretions

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40
Q

What drives apocrine secretion?

A

Adrenaline

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41
Q

During what situations does apocrine secretion occur?

A

stress, anxiety, pain, stimulation

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42
Q

Two types of hair

A

Vellus - short and fine (forehead)

Terminal - long and thick (axillae)

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43
Q

Bulb of hair

A

Enlargement at base of follicle

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44
Q

What kind of cells are at inferior aspect of bulb?

A

Matrix cells.

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45
Q

Explain proliferation and differentiation of matrix cells. What do they form?

A

Do so in a manner similar to basal cells of epidermis; form keratin of hair shaft

46
Q

What contributes to pigment of hair?

A

Melanocytes within matrix contribute to pigment

47
Q

What three parts make up hair shaft?

A

Medulla, Cortex, Cuticle

48
Q

Sebaceous gland attaches where?

A

To hair shaft

49
Q

Arrector pili muscle attaches where?

A

to hair bulb

50
Q

List layers of hair bulb from internal to external

A

hair matrix, inner root sheath, outer root sheath

51
Q

What is hair papilla?

A

contains blood vessels at base of hair bulb

52
Q

Type 1 pathogenic mechanism: type of response, what types of cells, which antibody, what are symptoms?

A

Immediate
Mast cells and basophils
IgE
Hives, bronchospasm, laryngeal, edema

53
Q

Type II pathogenic mechanism: type of response, which antibodies, what do antibodies react to and activate?

A

Cytotoxic
Circulating IgG or IgM
React to surface antigen and activate complement

54
Q

Type III pathogenic mechanism: type of response, how it works, which antibodies, physiological responses.

A

Immune complex
Antigen-antibody complexes deposit tissue causing inflammation
IgG or IgM
Chemotaxis of leukocytes, platelet damage, increased vascular permeability

55
Q

Type IV pathogenic mechanism: type of response, what type of immunity, when does it occur?

A

Delayed sensitivity
Cell mediated immunity
24-48 hours after exposure

56
Q

What is a dermoscopy? What does it help with?

A

Transilluminating light with magnification; helps identify distinguishable features in skin findings

57
Q

Exophytic

A

growth outward

58
Q

Indurated

A

dermal thickening

59
Q

Friable

A

bleeds easily with minimal trauma

60
Q

Invasive treatment options

A

Curettage, Electrodessication, cryotherapy, punch biopsy

61
Q 
Solar lentigo - known as \_\_\_\_\_\_ \_\_\_\_\_\_.
Caused by:
Common/uncommon.
Clinical presentation.
Tx.
A

age spots
local proliferation of melanocytes caused by UV damage to sun exposed areas
VERY common
Well circumscribed, small brown macule, often found in groups
No tx required.

62
Q 
Seborrheic Keratosis (SK)
What is it?
Benign/malignant.
When does it develop?
Is there a genetic link?
A

Benign epidermal lesion - proliferation of immature keratinocyte
After age 50 typically.
Genetic link to excess SKs

63
Q

Clinical presentation of SK. What is ISK?

A

Tan to black with warty, waxy appearance; well-demarcated; may have one or hundreds, found on cehst, beck, head, neck

ISK - irritated. Caused by rubbing or friction. May have pruritis, pain or bleeding.

64
Q

What is leser trlat sign? What is it possibly associated with? What other symptoms are often present?

A

sudden onset of multiple SKs with inflammatory base.
+ skin tags
+ acanthosis nigricans
Possible association with GI and lung cancers

65
Q

How to determine if it is SK?

Tx?

A

Biopsy maybe. Otherwise, clinical judgment.

Can remove for cosmetic reasons or some ISKs:
Cryotherapy, shave biopsy with 15 blade, curettage electrodessication

66
Q

Keratoacanthoma clinical presentation

A

rapid growth over 6-8 weeks

Round, flesh colored nodule with central keratin plug - often found in sun exposed areas

67
Q

Risk factors for keratoacantoma?

A

Middle age to elderly with fair skin; increased UV radiation or chemical carcinogens

68
Q

Management of keratoacantoma? What type of biopsy is preferred?

A

May resolve spontaneously in 6-9 months
Often requires biopsy and tx for dx.
Excisional biopsy

69
Q

Actinic Keratosis is known as

A

solar keratosis

70
Q

Actinic keratosis originates from

A

keratinocyte

71
Q

Actinic keratosis is considered __________. May progress to _____. What is the risk per year?

A

pre-cancerous
SCC - disease continuum
8% risk

72
Q

Risk factors for actinic keratosis

A

increased age, males more than females, light skin (Fitz 1, 2), chronic IV exposure, hx of sunburns, immunosuppression, genetic syndromes

73
Q

Fitzpatrick Scale

A

1 - very fair - always burns, never tans
2 - fair - usually burns, sometimes tans
3 - medium - sometimes burns, usually tans
4 - olive - rarely burns, always tans
5 - brown - rarely burns, tans easily
6 - dark brown - never burns, always tans

74
Q

Actinic keratosis clinical presentation

A

erythematous, scaly/gritty macule or papule

may be tender

75
Q

Subtypes and definitions of AK

A 
Hypertrophic - thickened
Atrophic - scale absent
AK with cutaneous horn
Pigmented
Actinic chelitis (lip)
76
Q

How to dx AK?
What is the differential dx?
How do you determine if it is AK or something else?
If lesion is _____ than 6 mm, consider _____.

A

clinical by visualization and touch
may need dermoscopy
shave or punch biopsy if unable to differentiate from SCC - lesion > 1cm, rapid grown, ulceration or pain associated
Greater; SCC in situ

77
Q

Tx of AK.
Spontaneously resolve?
Isolated lesions?
Multiple lesions?

A

Spontaneously resolves in 20-30% of cases but may reoccur

Isolated - cryotherapy or surgical intervention
Multiple - field tx == photodynamic therapy - topical photosensitizer selectively destroy target cells, topic 5-FU, imiquimod (aldara)

78
Q

AK prognosis

A

increased risk of non-melanoma skin cancer

routine skin check-ups every 6-12 months

79
Q

What is most common type of skin cancer?

A

BCC

80
Q

Why is it called BCC?

A

Arises from basal layer of epidermis.

81
Q

BCC clinical presentation

A 
nodular
flesh-colored or pinkish
pearly papule/nodeule
telanglectasia
central ulceration with rolled border (maybe)
common on head and neck

may also present superficial as pink patch similar to AK or SCC in situ. Pigmentation may also be present.

82
Q

BCC differential dx - 2 diseases

A

Sebaceous hyperplasia

Fibrous papule

83
Q

What is sebaceous hyperplasia? How do you differentiate sebaceous hyperpasia and BCC?

A

enlarged oil gland with central clearing; look for telanglectasia - BCC over lesion versis wrap around sebaceous hyperplasia

84
Q

What is fibrous papule? How do you differentiate it from BCC?

A

Benign angiofibroma
Skin-colored/pinkish papule on nose.
No telangiectasia and lacks pearly texture

85
Q

BCC tx - surgical

A

curettage and desiccation
cryotherapy
excision with 3-4mm margins
MOHS

86
Q

BCC tx - nonsurgical

A

Radiation

For superficial BCC - imiquimod cream, 5% fluorouracil cream, photodynamic therapy

87
Q

BCC prognosis

A

May recur so requires routine follow-up - 6-12 months with derm for two years and then self-exams; higher risk of developing non-melanoma skin cancers, metastasis is rare

88
Q 
SCC
Common?
Where does it originate from?
Most common sex and ages affected?
Risk factors?
A

2nd most common form of skin cancer
originates from keratinocytes
Males, 50-70 years old
Risk Factors - UV exposure, genetic alterations, chemical carcinogens; may arise in areas of previous trauma, skin injury

89
Q

SCC clinical presentation

A

Papule, plaque, or nodule
Pink, red or skin colored
Asymptomatic often, may be pruritic or tender
Lesion appears scaly, exophytic, indurated, and/or friable
Commonly appears warty

90
Q

Surgical tx for SCC

A

Wide excision - margins based on risk
MOHS
Curettage and desiccation or cryotherapy - SCC in situ

91
Q

Nonsurgical tx for SCC

A

Radiation - poor surgical candidates or residual tumor

SCC in situ - S- Fluorouracil therapy, imiquimod cream, diclofenac gel, ingenol mebutate, photodynamic therapy

92
Q

SCC prognosis
Rate of metastasis
Surveillance protocol

A

Rate of metastisis - 5%; rate increases if lesion is greater than 2 cm in diameter, greater than 4 mm deep, or recurrent

Surveillance - every 3-6 months x 2 years, then every 6-12 months x 3 years then annually for life

93
Q

MOHS - micrographic surgery
How do they determine margins?
What is the benefit of MOHS?

A

Tumor margins assessed in office to maximize tissue conservation; lowers recurrence rates

94
Q

Excisional v MOHS

A

Excisional - less expensive unless recurrence, faster, more providers offer tx

MOHS - complete margin analysis, higher cure rates, sparing of normal tissue, higher cost, longer appointment, subspecialist

95
Q

Malignant Melanoma
percentage of all skin cancers
average age of dx

A

3% of all skin cancers - high morbidity and mortality if not treated early

avg age of dx - 40; rare in children

96
Q

Risk factors for Malignant Melanoma

A

fair skin, blue eyes, blonde/red hair
>5 atypical nevi; >25 nevi, immunosuppression, personal or family history of melanoma, genetic predisposition in small percentage; prolong UV exposure - blistering sunburns, UVA exposure in tanning beds

97
Q

Clinical manifestation of melanoma

A

asymptomatic
most de novo with some arising from pre-existing nevus
pigmented papule, plaque, or nodule
ABCDEs

98
Q

Melanoma subtypes

A

Superficial spreading
Nodular
Lentigo Maligna
Acral Lentiginous

99
Q 
Superficial spreading melanoma
Common?
What layer of skin?
What population?
How does it spread?
Where is it commonly found in males and females?
A

most common subtype - 70%
confirmed to epidermis
younger population
radial spread is greater than vertical growh
Common on backs in males and back and legs in female s

100
Q

Nodular melanoma

A

Rapid verticle growth, little radial growth
Aggressive
Nodule is inflamed and friable

101
Q

Lentigo Maligna melanoma
Common in what population?
How does it progress?

A

elderly with chronic sun exposure

slow progression radially, rapid vertical growth - typically remains superficial

102
Q 
Acral lentiginous melanoma
What populations?
How does it spread?
Males or females?
What areas of the body?
A

darker skin; spreads superficial than vertical
more common in males than females
larger lesions due to delay in dx
palmar, plantar, or subungual

103
Q

Subungual

A

great toe or thumb
history of trauma
dark streak and involves proximal nail fold

104
Q

Amelanotic

A

minimal or absent pigment; extensive differential dx needed - psoriasis, dermatitis, BCC, SCC

105
Q

Biopsy of pigmented lesions

A

Photograph lesion prior to biopsy - document size and landmark

Biopsy entire lesion + 1-2 mm

106
Q

Melanoma prognosis
What to consider?
Who is at greatest risk of dying from melanoma?
Screening protocol.

A

Breslow depth, ulceration, mitotic rate, lymph node involvement

Greatest risk for lethal melanoma is males over 50 living alone. Screen high risk patients in PCP. Screening every 6 months for 2 years then annually.

107
Q

Melanoma tx

A

wide surgical excision - gold standard with 2 cm clear margins depending on depth of tumor at stage at dx

elective regional lymph node dissection/sentinel node biopsy

Advanced metastatic disease - chemotherapy

  • immunotherapy
  • gene therapy

Follow up every three months

108
Q

Chemotherapy to tx melanoma

A

used in combo with other agents

decarbazine and temozolomide

109
Q

immunotherapy to tx melanoma

A

adjunct therapy with interferon alfa (INFa)

110
Q

Melanoma prevention

A 
SPF 30+
Moisturizers with sunscreen
Full coverage - hats and sunglasses
Avoid sun 10 am-4pm
No tanning
Infants > 6 months should wear sunscreen and hats; better not to bring infants into sun if possible

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