Week 3 Flashcards
1
Q
What is cellulitis
A
Deep skin infection; infection invading the dermis and subcutaneous fat
2
Q
Most common causative organisms of cellulitis
A
Strep pyogenes
S aureus
Both can occur together
3
Q
Where does cellulitis usually occur
A
in the legs
4
Q
Risk factors for cellulitis
A
Diabetics / immunocompromised
Breaks in skin barrier
Fissured toes or heels
Venous insufficiency
Elderly
5
Q
What can cause breaks in skin barrier
A
Ulcers
Injuries
Psoriasis
Eczema
Ruptured blisters
6
Q
What condition can cause fissured toes or heels
A
Athlete’s foot
7
Q
Symptoms of cellulitis
A
Poorly demarcated erythema margins
Hot erythema
Swelling
Pain
Fever
Malaise
8
Q
Cellulitis is always unilateral/bilateral
A
unilateral
9
Q
Investigation for cellulitis
A
Clinical, use cultures if not sure
Blood culture
Skin swab - blisters fluid
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
11
Q
What antibiotics are used for cellulitis
A
Oral flucloxacillin
IV flucloxacillin if severe
12
Q
Alternative for oral flucloxacillin for mild-moderate cellulitis
A
Oral doxycycline
13
Q
Alternative for IV flucloxacillin for severe cellulitis
A
IV vancomycin
14
Q
What is a useful thing to do to check if the cellulitis is still spreading
A
Mark the margins of erythema
15
Q
What is impetigo
A
Superficial skin infection occurring at stratum corneum (immediately below the skin)
16
Q
Impetigo is most common in
A
Children
Infants
17
Q
Impetigo is most commonly caused by
A
S aureus
Strep pyogenes
18
Q
Symptoms of impetigo
A
Pruritus
Well defined lesions
Golden crust lesions with erythematous base
19
Q
Impetigo usually occur at
A
Face
20
Q
Investigations for impetigo
A
Clinical
Swab under certain conditions
21
Q
Under what conditions can you request for a skin swab for suspected impetigo
A
if the impetigo is
Severe
Recurrent
MRSA suspected
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
23
Q
Why should children with impetigo avoid sharing towels / remain good hygiene
A
Because impetigo is highly contagious
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
25
What is erysipelas
Infection of the dermis and UPPER subcutaneous tissue (more superficial than cellulitis)
26
Most erysipelas is caused by
Streptococcus pyogenes
27
Risk factors for erysipelas
Venous insufficiency
Immunocompromised
Breaks in skin barriers
Fissured toes / heels
Nasopharyngeal infections
28
Symptoms of erysipelas
Well demarcated, raised, swollen, erythematous, firm area
Fever
Systemic upset
29
Distribution of erysipelas
Mostly lower limbs
Butterfly distribution over the cheeks and bridge of nose
30
investigations for Erysipelas
Clinical
Cultures from entry of infection
Cultures from blister fluids
imaging if bone is suspected to be involved
31
Management for erysipelas
Rest
Analgesia
Elevate
Antibiotics
- Oral flucloxacillin
- IV flucloxacillin if severe
32
Describe the antibiotics used for erysipelas
Oral flucloxacillin
IV flucloxacillin if severe
33
Alternative for oral flucloxacillin for erysipelas
Erythromycin
34
What is necrotising fasciitis
Life threatening infection of subcutaneous tissue with spread along the fascial planes but not underlying muscles
35
Necrotising fasciitis causes extensive necrosis of
Superficial fascia
Subcutaneous fat
36
There are 4 types of necrotising fasciitis. Which ones are the most common
Type 1 - polymicrobial infection
Type 2 - mono microbial infection
37
What is type 1 necrotising fasciitis caused by
Different anaerobes
38
What is type 2 necrotising fasciitis caused by
Group A streptococci
39
Risk factors for necrotising fasciitis
Immunocompromised
Obesity
Person who inject drugs
Injuries
Peripheral arterial disease
40
Symptoms of necrotising fasciitis
Systemically unwell - tachycardia / tachypnea / pyrexic / hypotensive
Rapidly spreading diffuse erythema
Blisters
Oedema
Very painful
Purple discolouration
Crepitus over site
41
What may be the only sign in early stage of necrotising fasciitis
Mild oedema
42
Investigations for necrotising fasciitis
Blood cultures
Deep tissue cultures
43
Management for necrotising fasciitis
Urgent surgical debridement
Broad spectrum antibiotics
44
How do cancer cells emerge
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
45
Describe clonal evolution
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
46
Function of proto-oncogene
Positively regulates normal cell division (i.e. causes cell division when needed)
47
What is the mutated form of proto-oncogene called
Oncogene
48
Proto-oncogene or oncogene drives tumour formation
Oncogene
49
Function of tumour suppressor gene
Under certain factors, triggers:
Cell cycle arrest
Cell apoptosis
DNA repair
Blocking angiogenesis
50
What factors can cause p53 to stop cell division
UV radiation
Lack of nucleotides
Hypoxia
Ionising radiation
51
Examples of proto-oncogenes
Ras
Raf
growth factor receptors
52
Example of tumour suppressor gene
p53
53
Describe how UV radiation may lead to rise of cancer
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
54
Types of UV light
UVC
UVB
UVA
55
Which UV light can pass through glass window
UVA
56
Which UV light is more damaging
UVB
57
Which UV light is blocked by the ozone layer
UVC
58
Which UV light has the longest wavelength
UVA
59
What can block UVA
Sunscreen
60
What can block UVB
Sunscreen
Window glass
61
Damage from UVA causes
Pigmentation
Skin cancer
Photoaging
62
Damage from UVB causes
Sunburn
Pigmentation
Skin cancer
Photoaging
63
Which UV light causes indirect DNA damage
UVA
64
Which UV light causes direct DNA damgage
UVB
65
Shorter wavelength UV light affects the skin more deeply / superficially so UVA/UVB penetrates the skin more deeply
Superficially
So UVA penetrates the skin more deeply (longest wavelength)
66
What factors causes UV light to increase risk of skin cancer
Damage to DNA
Immunosuppressive
67
How does chronic UV exposure cause immunosuppression
Keratinocytes and dendritic cells secrete IL-10 (immunosuppressive)
Langerhan cells lose antigen presenting ability
T cells with immune suppressive ability
68
What are the UVB induced DNA lesions
formation of covalent linkages between adjacent pyrimidines on the same DNA strand
69
What are the UVB signature mutations
CT
TT
70
UVB DNA lesions can be repaired by
Nucleotide excision repair (NER)
71
UVA DNA lesions can be repaired by
base excision repair (BER)
72
What are the 2 main types of skin cancer
Non-melanoma (keratinocyte skin cancer)
Melanoma
73
Which type of skin cancer is more likely to metastasise
Melanoma
74
What are the benign melanocytic lesions
Freckles (ephilides)
Actinic lentigenes
Naevi
75
Difference between benign and malignant melanocytic lesions
Benign ones
-well demarcated borders
-not changing rapidly
-even pigmentation
-symmetrical
76
What are freckles
Patchy increase in melanin after UV exposure
77
What causes freckles
1 defective copy of MC1R gene (which controls type of melanin produced)
78
Freckles are common in
fair skin
red heads
79
What are actinic lentigines (age / liver spots)
small, gray-brown spots common in elderly that appear due to UV exposure
80
Actinic lentigines are most commonly found on
face
dorsal hands
forearms
81
Histology of actinic lentigenes will show
epidermis with elongated rate ridges (epithelial extensions that extend to dermis)
Increase melanin and basal melanocytes
82
What are congenital melanocytes naevi
Visible pigmented lesions present at birth due to benign proliferation of melanocytes
83
Congenital melanocytic naevi type of naevus
Junctional naevus
84
What are junctional naevus
When melanocytes proliferate and form clusters at DEJ
85
What do congenital melanocytic naevi look like
flat
smooth surface
even pigmentation
86
Can congenital melanocytic naevi increase risk of melanoma
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
Common acquired naevus type of naevus
Compound
88
What are compound naevus
Naevus due to clusters of melanocytes at epidermal junction and dermis
89
What are intradermal naevus
Naevus due to clusters of melanocytes at dermis
90
Describe the presentation of dysplastic naevi
> 6mm
Irregular border
Asymmetry
Uneven pigmentation
May be bumpy
91
Difference between dysplastic naevi and melanoma
Dysplastic naevi is not cancerous yet but has high chance of developing into melanoma
92
What is sporadic dysplastic naevi
Dysplastic naevi that is not inherited and slightly raises the risk of malignant melanoma
93
Patient with familial dysplastic naevi often has
family history of melanoma
Inheritance of CDKN2A
94
What does it mean if a patient has inherited CDKN2A gene
High risk of developing many atypical naevi throughout their whole life
95
Which type of dysplastic naevi increases the risk of melanoma more
Familial dysplastic naevi
96
What is a difference in histology between dysplastic naevi and melanoma
Epidermis in dysplastic naevi does not show architectural atypia and cellular atypia whereas it does in melanoma
97
Use of ABCDE rule for melanoma
Refer urgently if any lesions present with any of the features
98
ABCDE features for melanoma
Asymmetry
Border irregularity
Colour variation
Diameter >6mm
Evolution over time
99
What other sign can be used to identify malignant lesion
Ugly duckling sign - any lesions that doesn't look like the others
100
Risk factors for melanoma
Intermittent sun burn in childhood
Increasing age
Use of sun beds
Family history
Skin type 1
Dysplastic naevi
101
Melanoma mostly arise from
de novo - from normal skin
only 25% arise from pre-existing naevi
102
On which body parts do melanoma most commonly occur on
Sun exposed sites such as
Scalp
Face
Neck
Arm
Trunk
leg
103
Types of melanoma
Superficial spreading
Nodular
Lentigo Maligna
Acral lentingious
104
What are the 2 phases of growth of melanomas (except nodular melanoma)
Radial growth
Vertical growth
105
Nodular melanoma only has which growth phase
Vertical growth
106
Describe the 2 phases of growth of melanoma (except nodular)
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
Which type of melanoma is the most common
Superficial spreading melanoma
108
Superficial spreading melanoma is most commonly seen in
Trunk
Limbs
109
Which type of melanoma is the most aggressive one and why
Nodular melanoma because it only has vertical growth and no radial growth which allows metastasis
110
Which type of melanoma is usually presented late
Acral lentingious
111
Where does acral lentingious melanoma usually occur
Palms
Soles of feet
112
What is lentigo maligna melanoma
Melanoma that arise from pre-existing lentigo maligna
113
Where does lentigo maligna melanoma usually occur
Face
Scalp
Neck
114
Except from the skin, where else can melanoma occur and why
Eyes
Biliary tract
Meninges
Oesophagus
Anus
Due to abnormal migration of melanocytes in the embryo
115
Where do melanocytes migrate from during embryo stage
Neural crest
116
When should you suspect a lesion may be melanoma
New pigment lesion develops in adulthood
ABCDE
Ulceration
Bleeding
117
Investigation for melanoma
Narrow complete excision of lesion for biopsy
Breslow depth assessment
118
What is Breslow depth assessment
Measures the depth of tumour to assess the prognosis
119
Where should you measure from for breslow depth if the lesion is ulcerated
Base of ulcer to deepest tumour cell
120
What should be carried out to look for metastasis if breslow depth is > 1mm
Sentinel lymph node biopsy
121
Stage 1 melanoma breslow depth
<1 mm
122
Stage 2 melanoma breslow depth
1-2 mm
123
Stage 3 melanoma breslow depth
3-4 mm
124
Stage 4 melanoma breslow depth
> 4 mm
125
Management of melanoma
Stage 0 - 2 : wide excision to remove all tumour cells
Stage 3, 4: chemo, immunotherapy, genetic therapies
126
What are the genetic therapies
Imatinib
Debrafenib/vemurafenib
127
What is seborrheic keratosis
Benign epidermal lesion caused by proliferation of epidermal keratinocytes
128
Seborrheic keratosis is more common in which age group
Elderly, ageing skin
129
Seborrheic keratosis commonly present on
Face
Trunk
130
Appearance of seborrheic keratosis
Brown
Waxy surface
Warts and depressions on surface
Slightly raised
Well demarcated
131
What is Leser Trelat sign
Sudden emergence of many seborrhoeic keratosis which is associated to certain cancers
132
Which cancers are associated to Leser Trelat sign
Adenocarcinoma of stomach / colon
Squamous cell carcinoma
Lymphoma
Leukemia
133
What may be seen in histology of seborrheic keratosis
Horn cysts
Acanthosis
134
How are seborrheic keratosis managed
nothing usually unless patient wants it to be removed
Investigate further if leser trelat sign
135
What are the premalignant conditions of squamous cell carcinoma
Actinic keratosis
Bowen's disease
136
Premalignant conditions of SCC all causes which histological feature
Squamous dysplasia
137
Cause of actinic keratosis
Chronic sun exposure damaging DNA
138
Risk factors of actinic keratosis
Type I or II skin
History of sunburn
Outdoor occupation or hobbies
Immunosuppression
139
Histology presentation of actinic keratosis
Partial thickness squamous dysplasia of epidermal keratinocytes
140
Presentation of actinic keratosis
scaly, erythematous papules or patches
feels rough
141
Where do actinic keratosis occur on
Sun exposed surfaces
- scalp
- face
- dorsum of hands
142
Around what proportion of patients with actinic keratosis develop into SCC
< 1%
143
Management of small actinic keratosis
If localised - curettage / cryotherapy / surgery
144
Management of large actinic keratosis
5-fluorouracil
+ NSAID or imiquimod
145
What is Bowen's disease
squamous cell carcinoma in situ - premalignant lesion that is confined to epidermis
146
Histology presentation of Bowen's disease
Full thickness squamous dysplasia of epidermal keratinocytes
147
Presentation of Bowen's disease
slowly enlarging, well-demarcated, scaly red patch/plaque with an irregular border
148
Bowen's disease most commonly present on
legs in women
torso in men
149
A variant of Bowen's disease affects
genital mucosa
150
The variant of Bowen's disease that affects the genital mucosa is linked to which diseases
HPV
HIV
151
Management of Bowen's disease
Cryotherapy
Curettage
surgery
5-fluorouracil
imiquimod / NSAID
