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Pathology Flashcards

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Dermatology Board Prep flashcards
1
Q

What type of epithelium is the epidermis?

A

Keratinised stratified squamous epithelium

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2
Q

Which epithelial layer contains prominent desmosomes?

A

Prickle cells layer

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3
Q

Which epithelial layer is rich in kerato-hyalin granules?

A

Granular layer

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4
Q

Which epithelial layer is a mitotic pool?

A

Basal cell layer

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5
Q

Where are melanocytes found?

A

Basal layer and dermo-epidermal junction

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6
Q

How do melanocytes look on histology?

A

Have a pale halo surrounding them

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7
Q

What is the function of menalocytes?

A

Transfer pigment to keratinocytes using dendritic processes

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8
Q

Where are Langerhan’s cells found?

A

Upper and mid epidermis

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9
Q

The dermis is made up of what?

A

Type 1 and 111 collagen, elastic fibres and ground substance

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10
Q

Which area of the dermis is thin and found just below the epidermis?

A

Papillary dermis

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11
Q

What area of the dermis makes up most of it and is made from thicker bundles of type I collagen?

A

Reticular dermis

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12
Q

Which part of the dermis contains the appendage structures?

A

Reticular dermis

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13
Q

What is the epidermal basement membrane made up of?

A

Laminin and collagen IV

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14
Q

What is hyperkeratosis?

A

Increased thickness of the keratin layer

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15
Q

What is parakeratosis?

A

Persistence of nuclei in the keratin layer

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16
Q

What is acanthosis?

A

Increased thickness of the epithelium

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17
Q

What is papillomatosis?

A

Irregular epithelial thickening

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18
Q

What is spongiosis?

A

Oedema fluid between cells increasing the prominence of prickles

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19
Q

If oedema between cells is severe, what will form?

A

Vesicles

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20
Q

What is the main spongiotic disease?

A

Eczema

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21
Q

Where is the damage in lichenoid disorders?

A

Basal layer (basement membrane)

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22
Q

Give two examples of licheniod disorders?

A

Lichen Planus and lupus

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23
Q

Vesiculo-bullous disorders are characterised by what? Give 3 examples.

A

Blistering: bullous pemphigoid, pemphigus vulgaris, dermatitis herpetiformis

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24
Q

What happens to the epidermis in psoriasis?

A

Increased turnover and hyperplasia

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25
Q

What is the Koebner phenomenon?

A

New lesions of psoriasis occurring at sites of trauma

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26
Q

In psoriasis, what mediates the attack on the keratin layer?

A

Complement which then attracts neutrophils

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27
Q

What is erythoroedema?

A

An acute form of psoriasis which is often caused by drugs and can affect the whole body

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28
Q

What will the rash look like in lichen planus?

A

Itchy, flat topped violet papules

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29
Q

Irregular saw-toothed acanthosis is associated with what condition?

A

Lichen planus

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30
Q

In lichen planus, there will be upper dermal infiltrate of what?

A

Lymphocytes

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31
Q

What are Wichen’s straie?

A

White stripes on the buccal mucosa seen in lichen planus

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32
Q

What is pemphigus?

A

A rare, autoimmune bullous disease normally in middle age with loss of integrity of epidermal cell adhesion

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33
Q

Pemphigus responds to treatment with what?

A

Steroids

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34
Q

What is the most common type of pemphigus?

A

Pemphigus vulgaris

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35
Q

Pemphigus vulgaris involves IgG antibodies against where?

A

Desmoglein 3 which maintains desmosomal attachments

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36
Q

What is the end result of pemphigus vulgaris?

A

Acantholysis (loss of cellular connections)

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37
Q

Where is the blister in bullous pemphigoid?

A

Subepidermal

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38
Q

Immunofluorescence shows what in bullous pemphigoid?

A

IgG and complement deposited around the basement membrane

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39
Q

If you send older lesions of bullous pemphigoid for histology, what can they mimic?

A

Pemphigus vulgaris

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40
Q

What bullous skin condition has a strong association with coeliac disease and HLA-DQ2?

A

Dermatitis herpetiformis

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41
Q

What will dermatitis herpetiformis cause?

A

Intensely itchy, symmetrical lesions

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42
Q

What is the hallmark of dermatitis herpetiformis?

A

Papillary dermal microabscesses

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43
Q

In dermatitis herpetiformis, there will be deposits of what in the dermal papillae?

A

IgA

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44
Q

The distribution of acne reflects what?

A

Sebaceous gland sites

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45
Q

Acne is caused by what?

A

Increased androgens at puberty

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46
Q

What causes the infection in acne?

A

Anaerobic bacteria- corynebacterium acnes

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47
Q

Where are common sites to get dermatitis herpetiformis?

A

Elbows, knees, buttocks

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48
Q

Rosacea is more common in which sex? What are some triggers?

A

Females: spicy food, alcohol, sunlight, stress

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49
Q

What happens in rosacea?

A

Recurrent facial flushing with visible blood vessels, pustules and thickening of the skin (rhinophyma)

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50
Q

Some cases of rosacea respond to what medication?

A

Tetracyclines

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51
Q

The presence of what might be noted in rosacea?

A

Follicular demodex mites

52
Q

Most malignant melanocytic tumours are due to what?

A

UV light

53
Q

What two types of skin tumour are exclusively epidermal?

A

BCC and SCC

54
Q

When can skin tumours kill you?

A

Below the basement membrane (in the dermis)

55
Q

Where can skin tumours reach once they are in the dermis?

A

Vessels and lymphatics which allow them to spread

56
Q

Once melanocytes settle in the skin they are usually situated where?

A

Basally

57
Q

Does the melanocyte ratio change depending on race?

A

No

58
Q

What does the melanocortin 1 receptor gene encode? What is the function of this?

A

Encodes MC1R protein which sits on the cell surface and determines the balance of pigment in skin and hair

59
Q

What do phaeomelanin and eumelanin cause?

A

Phaeomelanin- all hair colours except red

Eumelanin- red hair

60
Q

What turns phaeomelanin into eumelanin?

A

MC1R gene

61
Q

What does 1 defective copy of the MC1R gene cause?

A

Freckling

62
Q

What do 2 defective copies of the MC1R gene cause?

A

Freckling and red hair

63
Q

What are ephilides?

A

Freckles

64
Q

What causes freckles?

A

A patchy increase in melanin pigmentation after UV exposure, in individuals who are genetically predisposed

65
Q

Actinic lentigines (age spots) are related to what?

A

UV exposure causing increased melanin and basal melanocytes

66
Q

When are most melanocytic naevi acquired?

A

The first 2 decades

67
Q

What defines small and medium congenital naevi?

A

Small = < 2cm, Medium = 2-20cm

68
Q

What is the risk of melanoma in large congenital naevi?

A

10-15%, may need surgical excision

69
Q

Describe simple naevi?

A

Very common benign lesions with low malignant potential

70
Q

Acquired naevi develop throughout life. In childhood it is known as junctional- where are the melanocytes?

A

In clusters at the DEJ

71
Q

Acquired naevi develop throughout life. In adolescence it is known as compound- where are the melanocytes?

A

DEJ and dermis

72
Q

Acquired naevi develop throughout life. In adulthood it is known as intra-dermal- where are the melanocytes?

A

Entirely dermal

73
Q

Describe clinical features of dysplastic naevi?

A

Generally >6cm diameter, varied pigment, asymmetrical

74
Q

Describe sporadic dysplastic naevi?

A

Not inherited, one-several atypical naevi, slight raised risk of melanoma

75
Q

Familial cases of dysplastic naevi have a strong family history of melanoma. How are these inherited and what is the penetrance?

A

Autosomal, high penetrance

76
Q

How many atypical naevi are normally seen in an individual with familial dysplastic naevi? What is the risk of melanoma?

A

Lots of atypical naevi, 100% lifetime risk of melanoma

77
Q

On histology, dysplastic naevi can show what?

A

Large nuclei and signs of inflammation with possible fibrosis

78
Q

Halo naevi have a peripheral halo of depigmentation. How does this occur? What are they overrun by?

A

Damage to the melanocytes around the lesion, overrun by lymphocytes

79
Q

Blue naevi are found where in the skin? What do they consist of?

A

Entirely dermal, consist of pigment rich dendritic spindle cells

80
Q

Who do Spitz naevi occur in?

A

< 20 years, often in children

81
Q

Are Spitz naevi benign? What may be seen on histology?

A

Yes, you may see epidermal hyperplasia

82
Q

Which sex is more likely to get a melanoma? When is the peak incidence?

A

Females (2:1)- middle age

83
Q

Where are melanomas mostly seen?

A

On sun exposed sites

84
Q

Superficial spreading melanomas are commonest where?

A

Trunk and limbs

85
Q

Lentiginous melanomas are commonest where?

A

Palms, soles or mucosa

86
Q

Lentigo maligna type melanomas are seen where?

A

Sun damaged face, neck, scalp

87
Q

Where are nodular melanomas seen?

A

Can be anywhere but commonly trunk

88
Q

All types of melanoma except nodular, grow as what first?

A

Macules (before they invade the dermis)

89
Q

When can a melanoma metastasise?

A

When it is in the dermis (vertical growth phase)

90
Q

What type of melanoma does not have a radical growth phase?

A

Nodular

91
Q

What is Breslow depth?

A

The deepest tumour from the granular layer in mm

92
Q

Describe pTis, pT1, pT2, pT3, pT4?

A

Tis = melanoma in site, T1 = < 1mm, T2 = 1-2mm, T3 = 2-4mm, T4 = 4+mm

93
Q

Adding ‘b’ after any TNM staging implies what? What does this do to prognosis?

A

Ulceration- decreases prognosis

94
Q

What are some adverse indicators of melanoma?

A

High mitotic rate, lymphovascular invasion, satellites, lymph node involvement

95
Q

What is the main treatment of a melanoma?

A

Primary excision with clear margins (+/- lymphadenectomy)

96
Q

Some aural melanomas involve what mutation? What may this be treated with?

A

c-Kit- imatinib

97
Q

Melanomas on intermittently sun exposed skin may have what mutation?

A

BRAF

98
Q

What is BRAF? What happens if it is mutated?

A

A proto-oncogene, it drives cell proliferation by up regulating MEK and ERK

99
Q

What type of lesion looks ‘stuck on’ and is raised, but is completely benign?

A

Seborrhoeic keratosis

100
Q

Give 3 examples of precancerous squamous dysplasia?

A

Bowen’s disease, actinic keratosis, viral lesions

101
Q

What invasive malignancies are epidermal?

A

BCC and SCC

102
Q

What is seborrhoeic keratosis?

A

Benign proliferation of epidermal keratinocytes

103
Q

Where is seborrhoeic keratosis common?

A

Face and trunk

104
Q

What can seborrhoeic keratosis also be known as?

A

Basal cell papilloma

105
Q

Where does BCC occur? Who in?

A

Sun exposed sites in middle aged-older people

106
Q

How do basal cell carcinomas grow?

A

Slow growing, locally destructive

107
Q

Do BCCs commonly metastasise?

A

No, very rare

108
Q

How may BCCs kill?

A

Getting into the brain through the eye

109
Q

Superficial BCC may sometimes look like a patch of eczema, how can you tell that its not?

A

It will not go away with steroids

110
Q

What are BCCs often surrounded by?

A

Telangectasic vessels

111
Q

What is Bowen’s disease?

A

Squamous cell carcinoma in situ

112
Q

Which sex is more likely to get Bowen’s disease? Where is it likely to appear?

A

The lower leg in females

113
Q

How will Bowen’s disease look?

A

Scaly patch or plaque, irregular border

114
Q

What two conditions can cause stasis dermatitis?

A

BCC and Bowen’s disease

115
Q

Where does actinic keratosis appear?

A

Sun exposed sites, especially head and neck

116
Q

All precursors of SCC show what?

A

Squamous dysplasi

117
Q

Where are viral precursors of SCC most commonly seen?

A

Ano-genital skin

118
Q

What is erythroplasia of Queryat-Penile?

A

Bowen’s disease of the penis, associated with HPV

119
Q

What type of HPV is mostly associated with dysplasia of SCC?

A

Type 16

120
Q

What is the commonest presentation of SCC?

A

Elderly, sun exposed skin, UV implicated, following actinic keratosis

121
Q

What is the prognosis of SCC?

A

Good, locally invasive, low but definite risk of metastases

122
Q

SCC can occasionally arise following what?

A

Chronic leg ulcers, burns, chronic lupus vulgaris

123
Q

Xeroderma pigmentosum has a rare association with what?

A

SCC

124
Q

What sites of SCC have a worse prognosis?

A

Scalp, ear or nose

125
Q

Squamous cells should only be seen where?

A

Epidermis

126
Q

What is mycosis fungoides?

A

Cutaneous T cell lymphoma

Dermatology (15 decks)

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