Pathology Flashcards

1
Q

what is the epidermis mainly maid up of?

A

mainly maturing squamous cells

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2
Q

where is the mitotic pool located?

A

in the basal layer

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3
Q

where are melanocytes found?

A

at the DEJ

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4
Q

what is epidermis?

A

stratified keratinising squamous epithelium

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5
Q

what are prominent in prickle cells?

A

desmosomes

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6
Q

what is the granular layer rich in?

A

keratohyalin granules

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7
Q

what type of cells are present in the corneal layer?

A

differentiated keratinised cells

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8
Q

where are corneocytes shed from & what does this create?

A

shed from the surface of the epidermis to form house dust

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9
Q

what do melanocytes do?

A

synthesise melanin pigment

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10
Q

how is melanin pigment transferred to keratinocytes?

A

via dendritic processes

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11
Q

where are Langerhans cells found?

A

in upper & mid epidermis

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12
Q

what kind of cell are Langerhans cells?

A

dendritic

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13
Q

what do Langerhans cells do?

A

act as sentiniels monitoring environment for antigens

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14
Q

what’s the difference between black people’s melanocytes & white people’s?

A

black people’s melanocytes make more melanin

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15
Q

what is the dermis made up of?

A

matrix of type 1 & type 111 collagen

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16
Q

what is present in the dermis?

A

elastic fibres

ground substance

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17
Q

what is ground substance?

A

hyaluronic acid & chondroitin sulphate

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18
Q

describe papillary dermis & where it is found?

A

thin layer just beneath the epidermis

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19
Q

describe reticular dermis

A

thicker bundles of type 1 collagen

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20
Q

what does reticular dermis contain?

A

appendage structures e.g. sweat glands, pilosebaceous units

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21
Q

what is the epidermal BM made of?

A

laminin & collagen 4

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22
Q

can you see Langerhan’s cells using a normal stain?

A

no

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23
Q

what is hyperkeratosis?

A

increased thickness of keratin layer

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24
Q

what is parakeratosis?

A

persistence of nuclei in the keratin layer

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25
what does parakeratosis indicate?
skin is turning over too quickly
26
what is acanthuses?
increased thickness of the epithelium
27
what is papillomatosis?
irregular epithelial thickening
28
what is spongiosis?
oedema fluid between squares appears to increase the prominence of intercellular prickles
29
what does severe spongiosis cause?
vesicles filled by oedema fluid
30
what are the 4 main inflammatory reaction patterns?
- spongiotic - psoriasiform - lichenoid - vesiculobullous
31
describe what happens in the spongiotic inflammatory reaction pattern & give an example
intraepidermal oedema | e.g. eczema
32
describe what happens in the psoriasiform inflammatory reaction pattern & give an exampl
elongation of the rate ridges | e.g. psoriasis
33
describe what happens in the lichenoid inflammatory reaction pattern & give an exampl
basal layer damage | e.g. lichen planus & lupus
34
describe what happens in the vesiculobullous inflammatory reaction pattern & give an exampl
blistering | e.g. bullous pemphigoid, pemphigus & dermatitis herpetiforms
35
what happens in psoriasis?
pathogenesis remains elusive - epidermal hyperplasia - hereditary factors? - new lesions at sites of trauma - complement mediated attack on keratin layer
36
if you were to scrape a scale of a psoriasis plaque, what would happen?
pinprick bleeding
37
what are crumbly nails in psoriasis due to?
dystrophy due to increased turnover in their epithelial nail beds
38
what does the distribution of acne vulgarise reflect?
sebaceous gland sites | - face, upper back, anterior chest
39
what is released when acne spots burst?
sebum & keratin which is very irritating for the skin
40
what can you stain for in acne vulgaris?
androgen receptors
41
what does keratin plugging of pilosebaceous units cause?
distension 7 then infection of the unit
42
where is sebum produced?
by the sebaceous gland
43
what is an open comedone?
blackhead
44
what is a closed comedone?
whitehead
45
in which sex is rosacea more common?
females
46
what is rosacea?
recurrent facial flushing, visible blood vessels, pustules, thickening of skin
47
what is rhinophyma?
thickening of skin
48
namesake known triggers of rosacea
sunlight alcohol spicy foods stress
49
which antibiotics does some rosacea respond to?
tetracyclines
50
what pathology is found in rosacea?
``` vascular ectasia pachy inflammation with plasma cells pustules perifollicular granulomas follicular demodex mites ```
51
where are demodex mites usually found?
in sebaceous duct
52
what happens around the mites?
lots of granulomatous inflammation
53
what is the primary feature of immunobullous disease?
blisters
54
what is pemphigus?
rare autoimmune bullous disease of variable severity
55
what causes pemphigus?
loss of integrity of epidermal cell adhesion
56
which drugs does pemphigus respond to?
steroids
57
how many distinct subtypes are there of pemphigus?
4, separable clinically & histologically
58
which is the most common subtype of pemphigus?
pemphigus vulgaris
59
what happens in pemphigus vulgaris?
IgG auto-antibodies are made against desmogelin 3
60
what does desmoglein 3 normally do?
maintains desmosomal attachments
61
what is the end result of pemphigus vulgaris?
acantholysis
62
where is pemphigus vulgaris affect in particular?
scalp, face, axillae, groin trunk
63
where can pemphigus vulgaris affect aside from the skin?
mucosa | e.g. motuh, resp. tract
64
when the blisters of pemphigus vulgaris rupture, what's left?
shallow erosions
65
what is common to all variants of pemphigus?
the process of acantholysis
66
what is pacantholysis?
lysis of intercellular adhesion sites
67
what kind of blisters are found in bullous pemphigoid?
subepidermal
68
what is the difference between bullous pemphigoid & pemphigus?
no acantholysis in bullous pemphigoid
69
what happens in bullous pemphigoid?
Circulating antibodies (IgG) react with a major and/or minor antigen of the hemidesmosomes anchoring basal cells to basement membrane
70
what does bullous pemphigoid result in?
local complement activation & tissue damage
71
what do older lesions of bullous pemphigoid show & what does this mimic?
show re-epithelialisation of their floor, mimicking pemphigus vulagris
72
what is dermatitis herpetiforms?
autoimmune bullous disease
73
which GI disease is dermatitis herpetiforms strongly associated with?
coeliac disease
74
what do the lesions in dermatitis herpetiforms look & feel like?
intensely itchy symmetrical lesions | found on elbows, knees & buttocks, often excoriated
75
what is the hallmark of dermatitis herpitforms?
papillary dermal microabscesses
76
in dermatitis herpetiforms, what forms in dermal papillae & what does this cause?
immune complexes | activates complement & generates neutrophil chemotaxins
77
where are melanocytes derived from?
the neural crest
78
where do the the melanoblasts migrate from & to during embryogenesis?
from neural crest to skin, uveal tract & leptomeninges
79
when do melanoblasts form melanocytes?
once they settle in the skin
80
where are the melanocytes situated?
basally situated
81
what is the ratio of melanocytes to basal keratinocytes?
1:5 - 1:10 | in all races
82
what does the MC1R gene encode?
MC1R protein which sits on cell surface?
83
what does the MC1R protein do?
determines balance of pigment in skin & hair | turns phaeomelanin into eumelanin
84
which protein causes red hair?
phaeomelanin
85
which protein is found in hair colours other than red?
eumelanin
86
what does one defective copy of MC1R cause?
freckling
87
what does two defective copy of MC1R cause?
red hair & freckling
88
when do freckles (ephilides) occur?
after UV exposure
89
what do freckles reflect?
clumpy distribution of melanocytes
90
what are actinic lentigines also known as?
solar lentigines | age/liver spots
91
what are actinic lentigines related to?
UV exposure
92
where are actinic lentigines usually found?
race, forearms & dorsal hands
93
what are actiniclentigines?
epidermis elongated with rite ridges & increased melanin & basal melanocytes
94
what are melanocytic naevi?
broad range of lesions which are either congenital or acquired
95
when are most naevi acquired?
in the first 2 decades of life
96
why do melanocytic naevi often have a hairy surface?
due to proliferation of hair follicles
97
what happens during infancy that allows the formation of simple naevi?
the melanocytes:keratinocyte ratio breaks down at a number of cutaneous sites
98
what are simple naevi?
very common being lesions with low malignant potential
99
which children have more naevi?
immunosuppressed/leukaemic
100
generally how big are dysplastic naevi?
> 6 mm diameter
101
what kind of pigment do dysplastic naevi usually have?
variegated pigment
102
what are dysplastic naevi borders normally like?
asymmetrical
103
which 2 clinical settings are dysplastic naevi usually found in?
- sporadic | - familial
104
describe the sporadic clinical setting
not inherited one to several atypical naevi risk of malignant melanocyte slightly raised
105
describe the familial clinical setting
strong FH of melanoma autosomal inheritance high penetrance lots of atypical naevi
106
what kind of atypia do dysplastic naevi exhibit?
architectural & cellular
107
what will be seen pathologically in a dysplastic naevi?
host-reaction fibrosis & inflammation, epidermis will not be affected
108
what do halo naevi look like?
brown with a peripheral halo of depigmentation
109
what do halo naevi look like pathologically?
inflammatpry regressioon & overrun by lymphocytes
110
describe blue naevi pathologically
entierly dermal & consist of pigment rich dendritic spindle celss
111
what cellular variant can blue naevi have?
may have mitoses & mimic melanoma
112
what do Spitz naevi consist of?
spindle and/pr epitheloid cells
113
what can Spitz naevi mimic?
melanoma
114
are malignant melanoma more common in males or females?
females
115
what age group does incidence of malignant melanoma peak in?
middle-age
116
what sites of the body are malignant melanoma usually found?
sun exposed sites
117
what factors would make you suspect a malignant melanoma?
- change in shape - irregular pigmentation - bleeding - development of satellite nodules - ulceration - new pigmented lesion develops in adulthood
118
what are the 4 main types of melanoma?
- superficial spreading - acral/mucosal lentignous - lentigo maligna - nodular
119
what is the commonest type of melanoma?
superficial spreading
120
where is superficial spreading melanoma usually found?
trunk & limbs
121
where are lentigo maligna usually found?
sun-damaged face/neck/scalp
122
where are nodular malignant melanoma usually found?
varied sites but often trunk
123
if a tumour regresses because of a host's immune system, what is there still a risk of?
metastases
124
what is the radial growth phase (RGP)?
malignant melanoma grows as a macule when either entirely in-situ or with dermal micro invasion, does not invade blood vessels at this point
125
what is vertical growth phase (VGP)?
eventually the melanoma cells invade the dermis forming an expansile mass with mitoses
126
in which growth phase can malignant melanoma metastasise?
VGP
127
what is nodular melanoma?
simple nodule of VGP tumour, some consider this more aggressive
128
what does melanoma prognosis relate to?
Breslow depth & ulceration
129
what is the Breslow depth?
the deepest part of the tumour from the granular layer in mm
130
how melanoma treated?
- primary excision to give clear margins - some receive a sentinel node biopsy - chemo, immunotherapy, genetic therapies
131
what are the epidermal tumours?
- seborrheic keratosis - Bowen's disease - actinic keratosis - viral lesions - basal & squamous cell carcinoma
132
what is a seborrheic keratosis?
benign proliferation of epidermal keratinocytes
133
what is the Leser-Trelat sign?
eruptive appearance of many lesions may indicate internal malignancy
134
what is a horn cyst?
not acutely a cyst but some fluid encased under the epidermis
135
what are the 3 main subtypes of BCC?
- nodular - superficial - infiltrative (morphoeic)
136
what does a BCC look like?
stuck shiny & pearly telangiectasis
137
what are the precursors of SCC?
- Bowen's disease (legs) - Actinic keratosis (head/neck) - Viral lesions (anogenital skin)
138
wha do precursors show?
squamous dysplasia
139
what does Bowen's disease look like?
scaly patch/plaque, irregular border, no dermal invasion
140
what is the commonest clinical setting for a SCC?
elderly, sun exposed sites, UV implicated
141
how can an SCC occasionally arise?
- chronic leg ulcers e.g. stasis ulcers - sites of burns; sinuses e.g. chronic osteomyelitis - chronic lupus vulgaris
142
what are the rare associations an SCC can arise?
- xeroderma pigmentosum - dystrophic variant - epidermolysis bullosa
143
what is the normal behaviour of an SCC?
generally good prognosis, locally invasive, low but definite risk of metastasis