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Dermatology > Pathology of Skin > Flashcards

Pathology of Skin Flashcards

1
Q

What is the peidermis mainly made up of

A

Maturing squamous cells

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2
Q

Where are melanocytes found

A

At the dermo-epidermal junction and in the basal layer

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3
Q

What is the ratio of melanocytes to basal cells

A

1:10

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4
Q

What is the granular layer rich in

A

Keratohyalin granules

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5
Q

What is the corneal layer made up of

A

Differentiated keratinised cells

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6
Q

What happens to corneocytes

A

They are shed from the surface and cause house dust

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7
Q

How is pigment shown

A

Melanocytes transfer pigment to keratinocytes via dendritic processes

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8
Q

Where are the Langerhan cells located

A

In the upper and mid-epidermis

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9
Q

Why are Langerhans cells important

A

In initiating inflammation

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10
Q

What is the difference in melanocytes in a pale skinned person compared to a darker skinned person

A

They have the same number of melanocytes but darker skinned people make more melanin

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11
Q

The matrix of the dermis is made up of what

A

Type 1 and type 3 collagen

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12
Q

What colour is a) collagen when and b) elastin when stained

A

Collagen is pink and elastin is blue

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13
Q

What is the ground substance of the dermis made up of

A

Hyaluronic acid and chondriotin sulphate

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14
Q

Describe the appearance and location of the papillary dermis

A

Thin and lies just beneath the epidermis

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15
Q

Describe the appearance and location of the reticular dermis

A

Thicker than the papillary dermis and contains type 1 collagen

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16
Q

What does the reticular dermis contain

A

Appendage structures - sweat glands, pilosebaceous units

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17
Q

What is the epidermal Basment Membrane made of

A

laminin and collagen IV

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18
Q

What type of cells appear to have halos around them

A

Melanocytes

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19
Q

What is parakeratosis

A

Persistence of nuclei in the keratin layer - the skin turnover is too high

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20
Q

Define papillomatosis

A

irregular epithelial thickening

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21
Q

Give an example of papillomatosis

A

Acanthiosis nigricans

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22
Q

What are the 4 main reaction patterns of inflammatory skin diseases

A

Spongiotic-intraepidermal oedema (eczema)
Psoriasiform-elongation of the rete ridges (psoriasis)
Lichenoid-basal layer damage (pemphigoid, pemphigus and dermatitis herpetiformis)

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23
Q

What are Munro micro abscess

A

A collection of neutrophils and classsically psoriasis

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24
Q

Where are 3 common sites of acne

A

Face
Upper back
Anterior chest

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25
Q

What are open comedones

A

Blackhead since it is oxidised

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26
Q

What causes a yellow head

A

A build up of Sebum and keratine cloggasge

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27
Q

Describe the aetiology of acne

A

Increased androgens at puberty, increased angrogen sensitivity of sebaceious glands
keratin plugging of pilosebaceious units
infection with anaerobic bacterium corynebacterium acnes

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28
Q

Rosacea is more common in females than males. true or false

A

True

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29
Q

What are some common features of rosacea

A

Recurrent facial flushing
Visible blood vessels
Pustules
Thickening of skin - rhinophyma

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30
Q

What are some triggers of rosacea

A

Sunlight
Alcohol
Spicy foods
Stress

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31
Q

What are sometimes found in the hair follicles under the microscope in patients with rosacea

A

Demodex mite in the sebaceious glands

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32
Q

What 2 things occur as a secondary phenomenon in many skin disease

A

eczema
herpes virus infection
burns

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33
Q

what type of disease have blisters as the primary feature

A

Immunobullous diseases

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34
Q

What are 3 examples of immunobullous diseases

A

Pemphigus
Bullous pemphigoid
Dermatitis Herpetiformis

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35
Q

What histologically happens in pemphigus

A

Loss of integrity of epidermal cell adhesion

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36
Q

What is the general treatment for pemphigus

A

Steroids

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37
Q

Who is usually affected by pemphigus

A

Middle aged men or women

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38
Q

In simple terms, describe pemphigus

A

Rare autoimmune bullous disease which is a problem involving cell to cell adhesion

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39
Q

What is the end result in pemphigus vulgaris

A

Acantholysis

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40
Q

What forms on the cell surface of pemphigus vulgaris

A

Immune complexes

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41
Q

What is the role of desmoglein 3 in pemphigus vulgaris

A

It maintains desmosomal attachments

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42
Q

What does Pemphigus Vulgaris produce

A

Fluid filled blisters which rupture to form shallow erosions

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43
Q

What areas of the body are affected by Pemphigus Vulgaris

A 
Scalp
Face
Axillae
groin
Trunk
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44
Q

What process is common to all variants of pemphigus ?

A

Acantholysis (lysis of intercellular adhesion sites)

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45
Q

What is bullous pemphigoid

A

Subepidermal blister

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46
Q

What do the IgG antibodies do in Bullous pemphigoid

A

They react with a major and/or minor antigen of the hemidesmosomes anchoring basal cells to the basement membrane.

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47
Q

if you think a patient has presented with bullous pemphigoid, what should be done about it

A

Punch biopsy or elliptical incisional

48
Q

What type of disease is dermatitis herpetiformis

A

A relatively rare condition that is autoimmune bullous disease

49
Q

What areas of the body are affected by dermatitis herpetiformis

A

Elbows, knees and buttocks

50
Q

What does dermatitis herpatiformis have a strong association with

A

Ceoliac disease

51
Q

What haplotype is dermatitis herpetiformis

A

HLA-DQ2

52
Q

What is the presenting complaint of dermatitis herpetiformis

A

Intensely itchy lesions-symmetrical

53
Q

What is the hallmark of dermatitis herpetiformis

A

Papillary dermal microabscesses

54
Q

What do IgA antibodies target in dermatitis herpetiformis

A

Gliadin component of ggluten but cross react with connective tissue matrix proteins

55
Q

Immune complexes form in dermal papillae and do what?

A

Activate complement and generate neutrophil chemotaxins

56
Q

What components of the skin give rise to tumours

A

All of them

57
Q

Where are melanocytes derived from

A

Neural crest

58
Q

Early in embryogenesis what mirgrates from the neural crest to what 3 places

A

Melanoblasts to the:
skin
Uveal tract (of the eye)
Leptomeninges (coverings in the prain)

59
Q

once the melanoblasts have migrated and settled in the skin, what do they form

A

melanocytes

60
Q

How is pigment transfered

A

via dendritic processes of the melanocytes

61
Q

What gene is the determinant of what your pigmentation is like?

A

MC1R (Melanocortin 1 receptor)

62
Q

What does one defective copy of MC1R cause

A

Freckling

63
Q

What does two defective copies of the MC1R gene cause

A

Red hair and freckles

64
Q

What does MC1R do?

A

turn phaeomelanin into eumelanin

65
Q

What is the medical term for freckles

A

Ephilides

66
Q

What are epihilides

A

Patchy increase in melanin pigmentation

67
Q

What are Actinic lentigines?

A

Age or liver spots related to UV exposure

68
Q

Where are you likely to see Actinic lentigines

A

Face, forearms and dorsal hands

69
Q

In Actinic lentigines, What is there an increase in

A

Melanin and basal melanocytes

70
Q

Melanoocytic naevi may be 1 of two types. What are these

A

Congenital or acquired

71
Q

Why is a patient with melanocytic naevi at increased risk of developing melanoma

A

Based on the fact that they have so many increased melanocytes

72
Q

What allows the formation of simple naevi

A

During infancy the melanocytes: keratinocyte ratio breaks down at a number of cutaneous sites

73
Q

There are 3 types of naevi. What are these and where are the melanocytes

A

Junctional: clusters of cells at the DEJ
Compound: Junctional clusters and groups of cells in the dermis
Intradermal: entirely dermal

74
Q

What are the majority of naevi

A

Compound

75
Q

Describe a typical dysplastic naevi

A

Generally >6mm
Variegated pigment
Border asymmetry

76
Q

What is a sporadic dysplastic naevi

A

Not inherited
One to several atypical naevi
risk of MM slightly raised

77
Q

What is a familial dyplastic naevi

A

strong FH of melanoma
Autosomal inheritance
Lifetime risk of melanoma up to 100%

78
Q

What are the 2 subdivisions of rarer naevi

A

Halo naevi and blue naevi

79
Q

Describe halo naevi

A

They have a peripheral halo of depigmentation and show inflammatory regression and are overrun by lymphocytes

80
Q

Describe blue naevi

A

Entirely dermal and consist of pigment rich dendritic spindle cells - the cellular variant may have mitoses and mimic melanoma

81
Q

Most Spitz naevus are malignant. True or False

A

False - most are entirely benign

82
Q

What do Spitz naevi consist of?

A

Large spindle and or epitheliod cells

83
Q

The incidence of melanoma peak at what age

A

Middle age

84
Q

What are 6 red flag signs that make you suspect melanoma

A 
Change in shape
New pigmented lesion that develops in adulthood
Irregular pigmentation
Ulceration
Bleeding 
Development of satellite nodules
85
Q

What are the 4 main types of malignant melanoma

A

Superficial spreading
Acral/ mucosal
Lentigo maligna
Nodular

86
Q

What is the most common type of melanoma and where do they appear

A

Superficial spreading - commonest on the trunk and limbs

87
Q

What type of melanoma are common in sun bed users

A

Lentigo maligna melanoma

88
Q

What is Vertical Growth Phase

A

When the melanoma cells invade the dermis forming an expansile mass with mitoses

89
Q

Why is VGP important

A

Only tumours in the VGP can spread and kill

90
Q

What is different about nodular melanoma compared to the others

A

It has metastatic potential from the beginning and therefore is considered more aggressive

91
Q

What does melanoma prognosis largely relate to

A

Breslow depth and ulceration

Breslow= deepest tumour from granular layer mm

92
Q

What does the suffix a/b mean when staging melanomas

A 
a = no ulceration
b = ulceration
93
Q

Where are common sites of metastatic spread

A 
Skin/ soft tissue
Heart 
Lungs 
GI tract 
Liver
Brain
94
Q

What is the treatment for melanoma

A

Primary excision to give clear margins

sentinal node biopsy - if positive, regional lymphadenopathy

95
Q

What is used for the treatment for advanced melanoma

A

Chemo
Immunotherapy
Genetic therapies

96
Q

What is BRAF

A

an oncogene which drives cell proliferation

97
Q

What are 3 types of precancerous dysplasias

A

Bowen’s disease
actinic keratosis
Viral lesions

98
Q

What is seborrhoeic keratosis?

A

Benign proliferation of epidermal keratinocytes

99
Q

Where are common places to find seborrhoeic keratosis

A

Face and the trunk

100
Q

Describe the appearance of seborrhoeic keratosis

A

stuck on appearance - greasy hyperkeratotic surface

101
Q

What are the 3 main subtypes for BCCs

A

Nodular
Superficial
Infiltrative

102
Q

Where do basal cells arise from

A

Epidermis

103
Q

Histologically, superficial basal cell carcinomas often have what appearance

A

Picket Fence appearance

104
Q

Where does Bowen’s disease present

A

On the legs

105
Q

Where does Actinic keratosis present

A

On the head and neck

106
Q

Where do viral lesions present

A

Anogenital skin

107
Q

Histologically what do precursors of squamous cell carcinoma show

A

Dysplasia

108
Q

Describe Bowen’s disease

A

mostly affects females on their lower legs
Scaly pathc / plaque
Irregular border
No dermal invasion

109
Q

Describe the appearance of Actinic keratosis

A

Lots of wrinkles and scales, discrete plaques with crusty scale

110
Q

What virus are Viral precursors often associated with

A

HPV

111
Q

What type of HPV is associated with dysplasia

A

Type 16

112
Q

What is the behaviour of squamous carcinoma

A

Generally good prognosis
Locally invasive
Low but definite risk of metastasis

113
Q

What is the appearance of an angiosarcoma

A

Bluish purple often like a bruise and may bleed

114
Q

Merkel cell carcinoma almost never malignant . True or False

A

False they are very malignant

115
Q

What are Merkel cells

A

Pressure receptor cells in the skin

Dermatology (21 decks)

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