Skin Pathology Flashcards
1
Q
Where is the mitotic pool in normal skin?
A
basal layer
2
Q
What type of epithelium is the normal epidermis made up of?
A
stratified keratinising squamous epithelium
3
Q
What are the granules found in the granular layer?
A
keratohyalin
4
Q
What is the main feature in prickle cell layer?
A
prominent desmosomes
5
Q
How is pigment transfered to keratinocytes from the melanocytes?
A
dendritic processes
6
Q
Where are the langerhan cells found?
A
upper and mid-epidermis
7
Q
What are the 2 layers of the dermis?
A
papillary dermis
reticular dermis
8
Q
What is found in the reticular dermis?
A
appendage structures- sweat glands and pilosebaceous units
9
Q
What is hyperkeratosis?
A
increased thickness of keratin layer
10
Q
What is parakeratosis?
A
persistence of nuclei in the keratin layer
11
Q
What is acanthosis?
A
increased thickness of epithelium
12
Q
What is papillomatosis?
A
irregular epithelial thickening
13
Q
What is spongiosis?
A
oedema fluid between squames appears to increase prominence of intercellular prickles
14
Q
What can develop is the spongiosis is sever?
A
vesicles filled oedema fluid develop
15
Q
What are the 4 main reaction patterns of inflammatory skin disease?
A
spongiotic-intraepidermal oedema
psoriasiform
lichenoid
vesiculobullous
16
Q
What is psoriasiform?
A
elongation of the rete ridges (the squiggly line of the DEJ)
17
Q
What is lichenoid?
A
basal layer damage
18
Q
Give examples vesiculobullous blistering diseases?
A
pemphigoid; pemphigus and dermatits herpetiformis
19
Q
What is the Koebner phenomenon?
A
new lesions arising at the sites of trauma
20
Q
How is complement involved in psoriasis?
A
complement attracts neutrophils to the keratin layer which creates munro microabscesses
21
Q
How do lichenoid disorders appear?
A
itchy, flat topped violaceous papules
22
Q
What disease has irregular sawtooth acanthosis with basal damage?
A
lichen planus
23
Q
What are other lichenoid disorders aside from lichen planus?
A
erythema multiforme and toxic epidermal necrolysis
24
Q
What is the most common type of pemphigus?
A
pemphigus vulgaris
25
What happens histologically during pemphigus?
loss of integrity of epidermal cell adhesion
26
What drugs can be used to treat pemphigus?
steroid
27
What causes the loss of integrity of the epidermal cell adhesion in pemphigus vulgaris?
IgG auto-antibodies are made against desmoglien which disrupts the desmosomes and results in acantholysis (loss of intercellular adhesion)
28
What is acantholysis?
lysis of intercellular adhseion sites
29
What are the main areas of skin that pemphigus vulgaris affects?
scalp, face, axillae, groin and trunk
30
How does pemphigus vulgaris appear?
fliud filled blisters which rupture to form shallow erosions-dont really see bullae
31
Where are the blisters in terms of skin layers in bullous pemphigoid?
sub-epidermally
32
What is the pathogenesis of bullous pemphigoid?
IgG react with antigens on hemidesmosomes which anchor basal cells to the BM so epidermis floats away from BM and fliud and inflam cells go into that space (esp. eosinophils)
33
What disease is dermatitis herpetiformis associated with?
coeliac disease
34
Where does dermatitis herpetiformis typically affect?
elbows, knees and buttocks symmetrically
35
What is histological hallmark of dermatitis herpetiformis?
papillary dermal microabscesses
36
How does dermatitis herpetiformis present?
intensly itchy lesions which are often excoriated
37
What immunoglobulin is involved with dermatitis herpetiformis?
IgA- the IgA which targets the gliadin cross reacts with connective tissue matrix proteins
38
Why does acne appear at puberty?
androgen levels increase
39
What are the symptoms in rosacea?
recurrent facial flushing
visible blood vessels
pustules
thickening of skin-rhinophyma
40
What are the triggers for rosacea?
sunlight
alcohol
spicy foods
stress
41
What drug does rosacea respond to?
tetracyclines
42
What is often seen on pathology of rosacea?
follicular demodex mites
43
What is the Breslow thickness?
from the granular layer down to the deepest point of invasion
44
What is the ABCDE rule for diagnosing melanoma?
```
A-asymmetry
B-border irregularity
C-colour variation
D-diameter greater than 6mm
E-evolution/change
```
45
What is the ugly duckling sign?
Comparing a mole to see if it is similar to other moles on a patient as all naevi on one individual should all look similar, if not-suggests melanoma
46
What do basal cell carcinomas arise from?
the keratinocytes withing the basal layer of the epidermis
47
What do SCCs come from?
the suprabasal layers
48
What breslow thickness gives a 5 year survival of 50%?
greater than 4mm
49
How do BCCs usually present?
a translucent, slow-growing lump or non-healing ulcer
50
Are BCCs usually painful?
no
51
What are the visible features of a BCC?
```
pearly or translucent with a rolled edge
telaniectasia
central ulceration "rodent ulcer"
scaly plaque "superficial"
infiltrative "morphoeic"
```
52
What are the types of BCC?
```
nodular
rodent ulcer
superficial
morphoiec (infiltrative)
pigmented
```
53
Where do SCCs tend to arise?
sun-damaged skin
54
How do SCCs present?
warty or crusted lump or non-healing ulcer
55
Do SCCs tend to be painful?
yes
56
What are the precursor lesions for SCCs?
actinic keratoses and Bowen's disease (carcinoma-in-situ)
57
How does Bowen's disease appear?
erythematous plaque
58
What is Naevoid basal cell carinoma syndrome?
an autosomal dominant familial cancer syndrome that results in early onset and multiple BCCs
59
What leads to tumour cells not all being homogenous?
When cells have mulitple mutations, they are more unstable and so acquire mutations in parralel clonal expansion giving lots of cell types within a tumour
60
What are the hallmarks of cancer?
```
sustaining proliferation signalling
evading growth suppressors
activiating invasion and metastases
enabling replicative immortality (telomerase)
inducing angiogenesis
resisting cell death
```
61
What happens in oncogenic Ras signalling?
Ras does not need growth factors to be activated and so cell division and proliferation happen constantly. Ras is an oncogene.
62
What xeroderma pigmentosum?
A genetic condition where genes involved in the repair of DNA damage are mutated leading to extrememly increased risk of skin cancer
63
What chemicals increase the risk of non-melanoma skin cancer?
```
coal tar pitch
soot
creosote
petroleum products
shale oils
arsenic
```
64
What diseases increase the risk of malignant melanoma?
ulcerative colitis
| Crohn's disease
65
What UV radiation wavelengths are most implicated in skin cancer and aging?
UVB and UVA
66
How does UVB cause skin damage?
through direct DNA damage
67
How does UVA cause skin damage?
indirect oxidative damage of DNA bases- penetrates more deeply into the skin than UVB
68
What type of DNA damage does UV cause?
pyrimidine dimer (two adjacent bases bond on the same DNA strand) which leads to distortion of the DNA helix
69
What is the problem with unrepaired UV induced photoproducts?
Interfere iwth base pariing during DNA replication leading to mutations- polymerase usually will correctly guess the right bases but is error prone and may insert the wrong bases
70
What is the problem with having oxidised DNA bases?
It can mispair with bases causing point mutations
71
How is direct DNA daamge repaired?
nucleotide excision repair
72
What is the UV signiture mutation in direct DNA damage?
TT becomes CC
73
What base is oxidised in indirect DNA damage?
deoxyguanosine becomes 8-oxo-deoxyguanosine
74
How is indirect DNA damage repaired?
base excision repair
75
What is the typical mutation in indirect DNA damage?
C becomes A (point mutation)
76
How does UV radiation induce immunosuppression?
depletes langerhan cells
generates regulatroty T cells which have an immune suppressive activity
causes secretion of anti-inflam cytokines by macrohpages and keratinocytes
77
What is the other name for freckles
ephilides
78
What do freckles reflect about melanocytes in the skin?
Their clumpy distribution
79
What causes actinic lentigenes?
UV exposure
80
Where are actinic lentigenes found mainly?
face ; forearms; dorsum of hands
81
What is seen pathologically in actinic lentigines?
elongated rete ridges and increased melanin and melanocytes
82
What type of congenital melanocytic naevi have a 10-15% risk of melanoma?
large lesions (>20cm)- giant garment type
83
How are large congenital naevi treated?
staged surgical excision
84
What is the developmental stages in naevus growth?
junctional naevus
compound naevus
intradermal naevus
85
What happens in the junctional naevus?
meloancytes proliferate leading to clusters of cells at the DEJ
86
What is found in the compound naevus?
junctional clusters as well as groups of cells in the dermis
87
What is found in the intradermal naevus?
all junctional activity has caesed and all the cells are entirely dermal
88
What do dysplastic naevi look like?
generall >6mm diameter
variegated pigment
border asymmetry
89
What are the 2 types of dysplastic naevi?
sporadic and familial
90
What happens pathologically with dysplastic naevi?
architectural atypia and cellular atypia with a host reaction of fibrosis and inflammation
91
What is the difference between dysplastic naevi and melanoma histologically?
the epidermis is not effaced in dysplasia although severe dysplasia may be difficulat to differenciate from melaonma in situ
92
What is a halo naevi?
have a peripheral halo of depigmentation which show inflammatory regression and are overrun by lymphocytes
93
What is a blue naevi?
entirely dermal and consist of pigment rich dendirtitic spindle cells
94
What is a Spitz naevus?
a naevus that occurs in the under 20s and closely mimic melanoma but are usually entirely benign
95
What do Spitz naevi look like?
pink lumps due to the prominent vasculature, epidermal hyperplasia
96
Where is melanoma most commonly found?
sun-exposed sites: scalp, face, neck, arm, trunk. leg
97
What are some signs of melanoma?
```
change in shape; irregular pigmentation
bleeding
development of satellite nodules
ulceration
new pigmented lesion deveoped in adulthood
```
98
What are the 4 main types of melanoma?
superficial spreading
acral/muscosal lentiginous
lentigo maligna
nodular
99
What are the 2 phases of growth in melanoma?
radial growth phase (RGP) and vertical growth phase (VGP)
100
What happens during the radial growth phase?
grow as macules when either entirely in-situ or with dermal microinvasion
101
What happens during the vertical growth phase?
the melanoma cells invade the dermis forming an expansile mass with mitoses
102
What is there an absense of in nodular melanoma?
no clinical or microscopic evidence of RGP
103
What are the adverse prognostic indicators in melanoma?
breslows thickness
ulceration
high mitotic rate; lymphovascular invasion; satellites ; sentinel lymph node involvement
104
What causes satellite deposits of MM?
invasion of local dermal lmyphatics
105
What defines a small naevus?
less than 1.5cm
106
What is atypical or dysplasatic naevus syndrom?
relative risk of melanoma increases with number of atypical naevi (2x if 2; 6x if >6)
107
What is the most common type of melanoma?
superficial spreading
108
How does superficial spreading melanoma progress?
a macule with irregular border and colour which may have been increasing in size for years before developing a nodule (slow horizontal growth phase and rapid vertical growth phase)
109
How does nodular melanoma appear
blue-black or redskin coloured nodule which may be ulcerated or bleeding
110
How can you differentiate nodular from superficial spreading?
nodular medlanoma do not have any significant surrounding macular pigmentation
111
What is a lentigo maligna melanoma?
an invasive melanom developing within a lentigo maligna
112
What areas of the body does acral lentiginous melanoma affect?
palms, soles or nails
113
What is amelanotic melanoma?
absent or minimal visible pigment
114
How do seborrheic keratoses?
brown/black greasy lesions
that have a "stuck on" appearance
often "warty but may be flat"
115
How do dermatofirbroma appear?
deep (dermal), brown/grey, firm nodule (can be red)
116
What can cause dermatofibromas?
insect bites
117
What margin is given in excising melanoma?
1cm lateral margin for every 1mm depth invasion
118
What is a seborrhoeic keratosis?
benign proliferation of epidermal keratinocytes
119
What is seen on pathology of seborrhoeic keratosis?
epidermal acanthosis; hyperkeratosis; horn cysts
120
What are 3 precursors of SCC?
bowens disease
actinic keratosis
viral lesions
121
What do precursors of SCC show?
squamous dysplasia
122
What type of HPV is associated with dysplasia?
type 16
123
What sites are associated with worse prognosis with SCC?
scalp, ear, nose; perineural spread
