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Y2 Dermatology > Week 3 > Flashcards

Week 3 Flashcards

1
Q

What is cellulitis

A

Deep skin infection; infection invading the dermis and subcutaneous fat

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2
Q

Most common causative organisms of cellulitis

A

Strep pyogenes
S aureus
Both can occur together

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3
Q

Where does cellulitis usually occur

A

in the legs

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4
Q

Risk factors for cellulitis

A

Diabetics / immunocompromised
Breaks in skin barrier
Fissured toes or heels
Venous insufficiency
Elderly

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5
Q

What can cause breaks in skin barrier

A

Ulcers
Injuries
Psoriasis
Eczema
Ruptured blisters

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6
Q

What condition can cause fissured toes or heels

A

Athlete’s foot

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7
Q

Symptoms of cellulitis

A

Poorly demarcated erythema margins
Hot erythema
Swelling
Pain
Fever
Malaise

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8
Q

Cellulitis is always unilateral/bilateral

A

unilateral

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9
Q

Investigation for cellulitis

A

Clinical, use cultures if not sure
Blood culture
Skin swab - blisters fluid

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10
Q

Management for cellulitis

A

Rest
Elevation
Analgesia
Splint
Antibiotics
-Oral flucloxacillin / doxycycline
- IV flucloxacillin / IV vancomycin if severe
Remove dead tissue
Mark the margin of affected area to see if it is spreading

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11
Q

What antibiotics are used for cellulitis

A

Oral flucloxacillin
IV flucloxacillin if severe

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12
Q

Alternative for oral flucloxacillin for mild-moderate cellulitis

A

Oral doxycycline

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13
Q

Alternative for IV flucloxacillin for severe cellulitis

A

IV vancomycin

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14
Q

What is a useful thing to do to check if the cellulitis is still spreading

A

Mark the margins of erythema

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15
Q

What is impetigo

A

Superficial skin infection occurring at stratum corneum (immediately below the skin)

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16
Q

Impetigo is most common in

A

Children
Infants

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17
Q

Impetigo is most commonly caused by

A

S aureus
Strep pyogenes

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18
Q

Symptoms of impetigo

A

Pruritus
Well defined lesions
Golden crust lesions with erythematous base

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19
Q

Impetigo usually occur at

A

Face

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20
Q

Investigations for impetigo

A

Clinical
Swab under certain conditions

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21
Q

Under what conditions can you request for a skin swab for suspected impetigo

A

if the impetigo is
Severe
Recurrent
MRSA suspected

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22
Q

Management for impetigo

A

Topical fusidic acid
Oral flucloxacillin or clarithromycin
Avoid sharing towels
Do not attend school until completion of antibiotic treatment

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23
Q

Why should children with impetigo avoid sharing towels / remain good hygiene

A

Because impetigo is highly contagious

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24
Q

Difference between cellulitis and impetigo

A

Impetigo is contagious but cellulitis is not
Impetigo is superficial skin infection, cellulitis is deep skin infection
Cellulitis causes poorly demarcated erythema whereas impetigo causes well defined lesions
Cellulitis doesn’t usually cause lesions, it causes swelling and erythema
Cellulitis mainly occurs in legs whereas impetigo occurs in face
Cellulitis mainly in elderly / immunocompromised people whereas impetigo mainly in children

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25
Q

What is erysipelas

A

Infection of the dermis and UPPER subcutaneous tissue (more superficial than cellulitis)

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26
Q

Most erysipelas is caused by

A

Streptococcus pyogenes

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27
Q

Risk factors for erysipelas

A

Venous insufficiency
Immunocompromised
Breaks in skin barriers
Fissured toes / heels
Nasopharyngeal infections

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28
Q

Symptoms of erysipelas

A

Well demarcated, raised, swollen, erythematous, firm area
Fever
Systemic upset

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29
Q

Distribution of erysipelas

A

Mostly lower limbs
Butterfly distribution over the cheeks and bridge of nose

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30
Q

investigations for Erysipelas

A

Clinical
Cultures from entry of infection
Cultures from blister fluids
imaging if bone is suspected to be involved

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31
Q

Management for erysipelas

A

Rest
Analgesia
Elevate
Antibiotics
- Oral flucloxacillin
- IV flucloxacillin if severe

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32
Q

Describe the antibiotics used for erysipelas

A

Oral flucloxacillin
IV flucloxacillin if severe

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33
Q

Alternative for oral flucloxacillin for erysipelas

A

Erythromycin

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34
Q

What is necrotising fasciitis

A

Life threatening infection of subcutaneous tissue with spread along the fascial planes but not underlying muscles

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35
Q

Necrotising fasciitis causes extensive necrosis of

A

Superficial fascia
Subcutaneous fat

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36
Q

There are 4 types of necrotising fasciitis. Which ones are the most common

A

Type 1 - polymicrobial infection
Type 2 - mono microbial infection

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37
Q

What is type 1 necrotising fasciitis caused by

A

Different anaerobes

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38
Q

What is type 2 necrotising fasciitis caused by

A

Group A streptococci

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39
Q

Risk factors for necrotising fasciitis

A

Immunocompromised
Obesity
Person who inject drugs
Injuries
Peripheral arterial disease

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40
Q

Symptoms of necrotising fasciitis

A

Systemically unwell - tachycardia / tachypnea / pyrexic / hypotensive
Rapidly spreading diffuse erythema
Blisters
Oedema
Very painful
Purple discolouration
Crepitus over site

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41
Q

What may be the only sign in early stage of necrotising fasciitis

A

Mild oedema

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42
Q

Investigations for necrotising fasciitis

A

Blood cultures
Deep tissue cultures

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43
Q

Management for necrotising fasciitis

A

Urgent surgical debridement
Broad spectrum antibiotics

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44
Q

How do cancer cells emerge

A
  1. Originate from a single cell
  2. A genetic mutation causes the rise of cancer cells
  3. Series of mutations accumulate in successive generations (clonal evolution)
  4. Cell accumulates enough mutations to become cancerous
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45
Q

Describe clonal evolution

A
  1. All cancer cells originate from an initiating mutation (this mutation allows it to be cancerous)
  2. Clonal expansion occur -> more cells with the first mutation
  3. Another mutation occurred during expansion. This gives survival benefits to the cancer cell
  4. Clones of the first and second mutations produced and outcompetes the ones with only the first mutation
  5. Eventually accumulate enough mutations to make it cancerous
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46
Q

Function of proto-oncogene

A

Positively regulates normal cell division (i.e. causes cell division when needed)

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47
Q

What is the mutated form of proto-oncogene called

A

Oncogene

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48
Q

Proto-oncogene or oncogene drives tumour formation

A

Oncogene

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49
Q

Function of tumour suppressor gene

A

Under certain factors, triggers:
Cell cycle arrest
Cell apoptosis
DNA repair
Blocking angiogenesis

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50
Q

What factors can cause p53 to stop cell division

A

UV radiation
Lack of nucleotides
Hypoxia
Ionising radiation

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51
Q

Examples of proto-oncogenes

A

Ras
Raf
growth factor receptors

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52
Q

Example of tumour suppressor gene

A

p53

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53
Q

Describe how UV radiation may lead to rise of cancer

A
  1. UV radiation causes damage to cells
  2. normal p53 gene in cells detect the abnormality and induces cell apoptosis
  3. However, one of the damaged cells already has a faulty p53 gene so it does not undergo apoptosis
  4. This allows the cancerous cell to proliferate (clonal expansion), accumulating more mutations
  5. Causes cancer
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54
Q

Types of UV light

A

UVC
UVB
UVA

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55
Q

Which UV light can pass through glass window

A

UVA

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56
Q

Which UV light is more damaging

A

UVB

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57
Q

Which UV light is blocked by the ozone layer

A

UVC

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58
Q

Which UV light has the longest wavelength

A

UVA

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59
Q

What can block UVA

A

Sunscreen

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60
Q

What can block UVB

A

Sunscreen
Window glass

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61
Q

Damage from UVA causes

A

Pigmentation
Skin cancer
Photoaging

62
Q

Damage from UVB causes

A

Sunburn
Pigmentation
Skin cancer
Photoaging

63
Q

Which UV light causes indirect DNA damage

A

UVA

64
Q

Which UV light causes direct DNA damgage

A

UVB

65
Q

Shorter wavelength UV light affects the skin more deeply / superficially so UVA/UVB penetrates the skin more deeply

A

Superficially
So UVA penetrates the skin more deeply (longest wavelength)

66
Q

What factors causes UV light to increase risk of skin cancer

A

Damage to DNA
Immunosuppressive

67
Q

How does chronic UV exposure cause immunosuppression

A

Keratinocytes and dendritic cells secrete IL-10 (immunosuppressive)
Langerhan cells lose antigen presenting ability
T cells with immune suppressive ability

68
Q

What are the UVB induced DNA lesions

A

formation of covalent linkages between adjacent pyrimidines on the same DNA strand

69
Q

What are the UVB signature mutations

A

CT
TT

70
Q

UVB DNA lesions can be repaired by

A

Nucleotide excision repair (NER)

71
Q

UVA DNA lesions can be repaired by

A

base excision repair (BER)

72
Q

What are the 2 main types of skin cancer

A

Non-melanoma (keratinocyte skin cancer)
Melanoma

73
Q

Which type of skin cancer is more likely to metastasise

A

Melanoma

74
Q

What are the benign melanocytic lesions

A

Freckles (ephilides)
Actinic lentigenes
Naevi

75
Q

Difference between benign and malignant melanocytic lesions

A

Benign ones
-well demarcated borders
-not changing rapidly
-even pigmentation
-symmetrical

76
Q

What are freckles

A

Patchy increase in melanin after UV exposure

77
Q

What causes freckles

A

1 defective copy of MC1R gene (which controls type of melanin produced)

78
Q

Freckles are common in

A

fair skin
red heads

79
Q

What are actinic lentigines (age / liver spots)

A

small, gray-brown spots common in elderly that appear due to UV exposure

80
Q

Actinic lentigines are most commonly found on

A

face
dorsal hands
forearms

81
Q

Histology of actinic lentigenes will show

A

epidermis with elongated rate ridges (epithelial extensions that extend to dermis)
Increase melanin and basal melanocytes

82
Q

What are congenital melanocytes naevi

A

Visible pigmented lesions present at birth due to benign proliferation of melanocytes

83
Q

Congenital melanocytic naevi type of naevus

A

Junctional naevus

84
Q

What are junctional naevus

A

When melanocytes proliferate and form clusters at DEJ

85
Q

What do congenital melanocytic naevi look like

A

flat
smooth surface
even pigmentation

86
Q

Can congenital melanocytic naevi increase risk of melanoma

A

Yes but only if the naevi is very large. This is because large naevi = many melanocytes = increase chance that one of it may be cancerous

87
Q

Common acquired naevus type of naevus

A

Compound

88
Q

What are compound naevus

A

Naevus due to clusters of melanocytes at epidermal junction and dermis

89
Q

What are intradermal naevus

A

Naevus due to clusters of melanocytes at dermis

90
Q

Describe the presentation of dysplastic naevi

A

> 6mm
Irregular border
Asymmetry
Uneven pigmentation
May be bumpy

91
Q

Difference between dysplastic naevi and melanoma

A

Dysplastic naevi is not cancerous yet but has high chance of developing into melanoma

92
Q

What is sporadic dysplastic naevi

A

Dysplastic naevi that is not inherited and slightly raises the risk of malignant melanoma

93
Q

Patient with familial dysplastic naevi often has

A

family history of melanoma
Inheritance of CDKN2A

94
Q

What does it mean if a patient has inherited CDKN2A gene

A

High risk of developing many atypical naevi throughout their whole life

95
Q

Which type of dysplastic naevi increases the risk of melanoma more

A

Familial dysplastic naevi

96
Q

What is a difference in histology between dysplastic naevi and melanoma

A

Epidermis in dysplastic naevi does not show architectural atypia and cellular atypia whereas it does in melanoma

97
Q

Use of ABCDE rule for melanoma

A

Refer urgently if any lesions present with any of the features

98
Q

ABCDE features for melanoma

A

Asymmetry
Border irregularity
Colour variation
Diameter >6mm
Evolution over time

99
Q

What other sign can be used to identify malignant lesion

A

Ugly duckling sign - any lesions that doesn’t look like the others

100
Q

Risk factors for melanoma

A

Intermittent sun burn in childhood
Increasing age
Use of sun beds
Family history
Skin type 1
Dysplastic naevi

101
Q

Melanoma mostly arise from

A

de novo - from normal skin
only 25% arise from pre-existing naevi

102
Q

On which body parts do melanoma most commonly occur on

A

Sun exposed sites such as
Scalp
Face
Neck
Arm
Trunk
leg

103
Q

Types of melanoma

A

Superficial spreading
Nodular
Lentigo Maligna
Acral lentingious

104
Q

What are the 2 phases of growth of melanomas (except nodular melanoma)

A

Radial growth
Vertical growth

105
Q

Nodular melanoma only has which growth phase

A

Vertical growth

106
Q

Describe the 2 phases of growth of melanoma (except nodular)

A
  1. Radial growth: growing horizontally as macules not nodules. May invade the papillary layer of dermis
  2. Vertical growth: growth vertically and invading the dermis (deeper into the tissue), forming a tumour
107
Q

Which type of melanoma is the most common

A

Superficial spreading melanoma

108
Q

Superficial spreading melanoma is most commonly seen in

A

Trunk
Limbs

109
Q

Which type of melanoma is the most aggressive one and why

A

Nodular melanoma because it only has vertical growth and no radial growth which allows metastasis

110
Q

Which type of melanoma is usually presented late

A

Acral lentingious

111
Q

Where does acral lentingious melanoma usually occur

A

Palms
Soles of feet

112
Q

What is lentigo maligna melanoma

A

Melanoma that arise from pre-existing lentigo maligna

113
Q

Where does lentigo maligna melanoma usually occur

A

Face
Scalp
Neck

114
Q

Except from the skin, where else can melanoma occur and why

A

Eyes
Biliary tract
Meninges
Oesophagus
Anus
Due to abnormal migration of melanocytes in the embryo

115
Q

Where do melanocytes migrate from during embryo stage

A

Neural crest

116
Q

When should you suspect a lesion may be melanoma

A

New pigment lesion develops in adulthood
ABCDE
Ulceration
Bleeding

117
Q

Investigation for melanoma

A

Narrow complete excision of lesion for biopsy
Breslow depth assessment

118
Q

What is Breslow depth assessment

A

Measures the depth of tumour to assess the prognosis

119
Q

Where should you measure from for breslow depth if the lesion is ulcerated

A

Base of ulcer to deepest tumour cell

120
Q

What should be carried out to look for metastasis if breslow depth is > 1mm

A

Sentinel lymph node biopsy

121
Q

Stage 1 melanoma breslow depth

A

<1 mm

122
Q

Stage 2 melanoma breslow depth

A

1-2 mm

123
Q

Stage 3 melanoma breslow depth

A

3-4 mm

124
Q

Stage 4 melanoma breslow depth

A

> 4 mm

125
Q

Management of melanoma

A

Stage 0 - 2 : wide excision to remove all tumour cells
Stage 3, 4: chemo, immunotherapy, genetic therapies

126
Q

What are the genetic therapies

A

Imatinib
Debrafenib/vemurafenib

127
Q

What is seborrheic keratosis

A

Benign epidermal lesion caused by proliferation of epidermal keratinocytes

128
Q

Seborrheic keratosis is more common in which age group

A

Elderly, ageing skin

129
Q

Seborrheic keratosis commonly present on

A

Face
Trunk

130
Q

Appearance of seborrheic keratosis

A

Brown
Waxy surface
Warts and depressions on surface
Slightly raised
Well demarcated

131
Q

What is Leser Trelat sign

A

Sudden emergence of many seborrhoeic keratosis which is associated to certain cancers

132
Q

Which cancers are associated to Leser Trelat sign

A

Adenocarcinoma of stomach / colon
Squamous cell carcinoma
Lymphoma
Leukemia

133
Q

What may be seen in histology of seborrheic keratosis

A

Horn cysts
Acanthosis

134
Q

How are seborrheic keratosis managed

A

nothing usually unless patient wants it to be removed
Investigate further if leser trelat sign

135
Q

What are the premalignant conditions of squamous cell carcinoma

A

Actinic keratosis
Bowen’s disease

136
Q

Premalignant conditions of SCC all causes which histological feature

A

Squamous dysplasia

137
Q

Cause of actinic keratosis

A

Chronic sun exposure damaging DNA

138
Q

Risk factors of actinic keratosis

A

Type I or II skin
History of sunburn
Outdoor occupation or hobbies
Immunosuppression

139
Q

Histology presentation of actinic keratosis

A

Partial thickness squamous dysplasia of epidermal keratinocytes

140
Q

Presentation of actinic keratosis

A

scaly, erythematous papules or patches
feels rough

141
Q

Where do actinic keratosis occur on

A

Sun exposed surfaces
- scalp
- face
- dorsum of hands

142
Q

Around what proportion of patients with actinic keratosis develop into SCC

A

< 1%

143
Q

Management of small actinic keratosis

A

If localised - curettage / cryotherapy / surgery

144
Q

Management of large actinic keratosis

A

5-fluorouracil
+ NSAID or imiquimod

145
Q

What is Bowen’s disease

A

squamous cell carcinoma in situ - premalignant lesion that is confined to epidermis

146
Q

Histology presentation of Bowen’s disease

A

Full thickness squamous dysplasia of epidermal keratinocytes

147
Q

Presentation of Bowen’s disease

A

slowly enlarging, well-demarcated, scaly red patch/plaque with an irregular border

148
Q

Bowen’s disease most commonly present on

A

legs in women
torso in men

149
Q

A variant of Bowen’s disease affects

A

genital mucosa

150
Q

The variant of Bowen’s disease that affects the genital mucosa is linked to which diseases

A

HPV
HIV

151
Q

Management of Bowen’s disease

A

Cryotherapy
Curettage
surgery
5-fluorouracil
imiquimod / NSAID

Y2 Dermatology (5 decks)

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