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
2
Q
List the layers of the epidermis from superficial to deep
A
Stratum corneum Stratum lucidum Stratum Granulosum Stratum spinosum Stratum basale
3
Q
Feature of stratum corneum?
A
superficial layer with shedding dead skin
4
Q
Feature of stratum lucidum?
A
found on palmar and plantar surfaces
5
Q
Feature of stratum granulosum?
A
keratinization
6
Q
Feature of stratum spinosum?
A
spiny-shaped cells (strength and flexibility)
7
Q
Feature of stratum basale
A
Cells germinate - keratinocytes
8
Q
Types of cells within epidermis
A
keratinocytes, melanocytes, merkel cells, langerhans cells
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
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
11
Q
What cells are the macrophages of the skin and have an immunologic function?
A
Langerhan’s cells
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
13
Q
Which cells may have neuroendocrine function?
A
Merkel cells in epidermis
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
15
Q
What is the dermis?
A
Support structure that contains blood, lymph vessels, nerves, hair follicles, glands, and fibrous tissue
16
Q
Layers of dermis?
A
Papillary dermis - superficial
Reticular dermis - deep
Ground substance
17
Q
Papillary dermis contains
A
loose network of fine collagen
18
Q
Reticular dermis contains
A
densely packed and thick collagen bundles; elastic fibers are largely located here
19
Q
Ground substance contains
A
proteoglycans and glycosaminoglycans
20
Q
Basement membrane zone
A
dermal-epidermal junction and barrier for malignant cells
21
Q
Two layers of basement membrane zone
A
Basal lamina and reticular connective tissue
22
Q
Basal lamina layers
A
Lamina lucida and lamina densa
23
Q
Describe lamina lucida.
A
clear zone traversed by transmembranous proteins
24
Q
Describe lamina densa.
A
dense zone of type IV collagen derived from epidermal cells
25
Describe reticular connective tissue.
thick fibrous bands of type VII collagen connecting into dermis; anchoring fibrils
26
Defects in the Basement membrane zone are the basis for what type of diseases?
blistering
27
Hypodermis contains
fibroblasts, adipose, and macrophages
subcutaneous fat
larger vessels and nerves
28
Describe subcutaneous fat of hypodermis.
Deepest layer. network of collagen and fat cells. conserves heat and provides shock absorbency
29
What layer conserves heat and provides shock absorbency?
Subcutaneous fat of hypodermis layer
30
Eccrine gland function
Temperature regulation
31
What type of gland is eccrine gland and where is it located? What is its function?
Coiled gland in deep dermis for secretion
32
Straight duct extends to _______ to transport sweat to surface of skin
epidermis
33
Eccrine covers ____ of the body and releases at ____ of skin.
most, surface
34
How many eccrine glands are there? What is secretory capacity?
2-3 million
| 10 L/day secretory capacity
35
Eccrine - Sweat begins as _______ with plasma, however due to _______ reabsorption in duct, becomes ______
isotonic, electrolyte, hypotonic
36
Apocine glands secrete into ______
sac of hair follicles
37
Apocrine are concentrated in what two regions? Where are modified glands located?
Axillary and anogenital regions; modified glands in eyelids, breasts, ears
38
Apocrine glands release what kind of fluid?
thick, clear, odorless
39
Why does body odor occur?
bacteria acts upon apocrine secretions
40
What drives apocrine secretion?
Adrenaline
41
During what situations does apocrine secretion occur?
stress, anxiety, pain, stimulation
42
Two types of hair
Vellus - short and fine (forehead)
| Terminal - long and thick (axillae)
43
Bulb of hair
Enlargement at base of follicle
44
What kind of cells are at inferior aspect of bulb?
Matrix cells.
45
Explain proliferation and differentiation of matrix cells. What do they form?
Do so in a manner similar to basal cells of epidermis; form keratin of hair shaft
46
What contributes to pigment of hair?
Melanocytes within matrix contribute to pigment
47
What three parts make up hair shaft?
Medulla, Cortex, Cuticle
48
Sebaceous gland attaches where?
To hair shaft
49
Arrector pili muscle attaches where?
to hair bulb
50
List layers of hair bulb from internal to external
hair matrix, inner root sheath, outer root sheath
51
What is hair papilla?
contains blood vessels at base of hair bulb
52
Type 1 pathogenic mechanism: type of response, what types of cells, which antibody, what are symptoms?
Immediate
Mast cells and basophils
IgE
Hives, bronchospasm, laryngeal, edema
53
Type II pathogenic mechanism: type of response, which antibodies, what do antibodies react to and activate?
Cytotoxic
Circulating IgG or IgM
React to surface antigen and activate complement
54
Type III pathogenic mechanism: type of response, how it works, which antibodies, physiological responses.
Immune complex
Antigen-antibody complexes deposit tissue causing inflammation
IgG or IgM
Chemotaxis of leukocytes, platelet damage, increased vascular permeability
55
Type IV pathogenic mechanism: type of response, what type of immunity, when does it occur?
Delayed sensitivity
Cell mediated immunity
24-48 hours after exposure
56
What is a dermoscopy? What does it help with?
Transilluminating light with magnification; helps identify distinguishable features in skin findings
57
Exophytic
growth outward
58
Indurated
dermal thickening
59
Friable
bleeds easily with minimal trauma
60
Invasive treatment options
Curettage, Electrodessication, cryotherapy, punch biopsy
61
```
Solar lentigo - known as ______ ______.
Caused by:
Common/uncommon.
Clinical presentation.
Tx.
```
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
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Seborrheic Keratosis (SK)
What is it?
Benign/malignant.
When does it develop?
Is there a genetic link?
```
Benign epidermal lesion - proliferation of immature keratinocyte
After age 50 typically.
Genetic link to excess SKs
63
Clinical presentation of SK. What is ISK?
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
What is leser trlat sign? What is it possibly associated with? What other symptoms are often present?
sudden onset of multiple SKs with inflammatory base.
+ skin tags
+ acanthosis nigricans
Possible association with GI and lung cancers
65
How to determine if it is SK?
| Tx?
Biopsy maybe. Otherwise, clinical judgment.
Can remove for cosmetic reasons or some ISKs:
Cryotherapy, shave biopsy with 15 blade, curettage electrodessication
66
Keratoacanthoma clinical presentation
rapid growth over 6-8 weeks
| Round, flesh colored nodule with central keratin plug - often found in sun exposed areas
67
Risk factors for keratoacantoma?
Middle age to elderly with fair skin; increased UV radiation or chemical carcinogens
68
Management of keratoacantoma? What type of biopsy is preferred?
May resolve spontaneously in 6-9 months
Often requires biopsy and tx for dx.
Excisional biopsy
69
Actinic Keratosis is known as
solar keratosis
70
Actinic keratosis originates from
keratinocyte
71
Actinic keratosis is considered __________. May progress to _____. What is the risk per year?
pre-cancerous
SCC - disease continuum
8% risk
72
Risk factors for actinic keratosis
increased age, males more than females, light skin (Fitz 1, 2), chronic IV exposure, hx of sunburns, immunosuppression, genetic syndromes
73
Fitzpatrick Scale
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
Actinic keratosis clinical presentation
erythematous, scaly/gritty macule or papule
| may be tender
75
Subtypes and definitions of AK
```
Hypertrophic - thickened
Atrophic - scale absent
AK with cutaneous horn
Pigmented
Actinic chelitis (lip)
```
76
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 _____.
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
Tx of AK.
Spontaneously resolve?
Isolated lesions?
Multiple lesions?
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
AK prognosis
increased risk of non-melanoma skin cancer
routine skin check-ups every 6-12 months
79
What is most common type of skin cancer?
BCC
80
Why is it called BCC?
Arises from basal layer of epidermis.
81
BCC clinical presentation
```
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
BCC differential dx - 2 diseases
Sebaceous hyperplasia
| Fibrous papule
83
What is sebaceous hyperplasia? How do you differentiate sebaceous hyperpasia and BCC?
enlarged oil gland with central clearing; look for telanglectasia - BCC over lesion versis wrap around sebaceous hyperplasia
84
What is fibrous papule? How do you differentiate it from BCC?
Benign angiofibroma
Skin-colored/pinkish papule on nose.
No telangiectasia and lacks pearly texture
85
BCC tx - surgical
curettage and desiccation
cryotherapy
excision with 3-4mm margins
MOHS
86
BCC tx - nonsurgical
Radiation
For superficial BCC - imiquimod cream, 5% fluorouracil cream, photodynamic therapy
87
BCC prognosis
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
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SCC
Common?
Where does it originate from?
Most common sex and ages affected?
Risk factors?
```
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
SCC clinical presentation
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
Surgical tx for SCC
Wide excision - margins based on risk
MOHS
Curettage and desiccation or cryotherapy - SCC in situ
91
Nonsurgical tx for SCC
Radiation - poor surgical candidates or residual tumor
| SCC in situ - S- Fluorouracil therapy, imiquimod cream, diclofenac gel, ingenol mebutate, photodynamic therapy
92
SCC prognosis
Rate of metastasis
Surveillance protocol
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
MOHS - micrographic surgery
How do they determine margins?
What is the benefit of MOHS?
Tumor margins assessed in office to maximize tissue conservation; lowers recurrence rates
94
Excisional v MOHS
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
Malignant Melanoma
percentage of all skin cancers
average age of dx
3% of all skin cancers - high morbidity and mortality if not treated early
avg age of dx - 40; rare in children
96
Risk factors for Malignant Melanoma
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
Clinical manifestation of melanoma
asymptomatic
most de novo with some arising from pre-existing nevus
pigmented papule, plaque, or nodule
ABCDEs
98
Melanoma subtypes
Superficial spreading
Nodular
Lentigo Maligna
Acral Lentiginous
99
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Superficial spreading melanoma
Common?
What layer of skin?
What population?
How does it spread?
Where is it commonly found in males and females?
```
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
Nodular melanoma
Rapid verticle growth, little radial growth
Aggressive
Nodule is inflamed and friable
101
Lentigo Maligna melanoma
Common in what population?
How does it progress?
elderly with chronic sun exposure
| slow progression radially, rapid vertical growth - typically remains superficial
102
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Acral lentiginous melanoma
What populations?
How does it spread?
Males or females?
What areas of the body?
```
darker skin; spreads superficial than vertical
more common in males than females
larger lesions due to delay in dx
palmar, plantar, or subungual
103
Subungual
great toe or thumb
history of trauma
dark streak and involves proximal nail fold
104
Amelanotic
minimal or absent pigment; extensive differential dx needed - psoriasis, dermatitis, BCC, SCC
105
Biopsy of pigmented lesions
Photograph lesion prior to biopsy - document size and landmark
Biopsy entire lesion + 1-2 mm
106
Melanoma prognosis
What to consider?
Who is at greatest risk of dying from melanoma?
Screening protocol.
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
Melanoma tx
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
Chemotherapy to tx melanoma
used in combo with other agents
| decarbazine and temozolomide
109
immunotherapy to tx melanoma
adjunct therapy with interferon alfa (INFa)
110
Melanoma prevention
```
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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