Week 3 Flashcards
What is cellulitis
Deep skin infection; infection invading the dermis and subcutaneous fat
Most common causative organisms of cellulitis
Strep pyogenes
S aureus
Both can occur together
Where does cellulitis usually occur
in the legs
Risk factors for cellulitis
Diabetics / immunocompromised
Breaks in skin barrier
Fissured toes or heels
Venous insufficiency
Elderly
What can cause breaks in skin barrier
Ulcers
Injuries
Psoriasis
Eczema
Ruptured blisters
What condition can cause fissured toes or heels
Athlete’s foot
Symptoms of cellulitis
Poorly demarcated erythema margins
Hot erythema
Swelling
Pain
Fever
Malaise
Cellulitis is always unilateral/bilateral
unilateral
Investigation for cellulitis
Clinical, use cultures if not sure
Blood culture
Skin swab - blisters fluid
Management for cellulitis
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
What antibiotics are used for cellulitis
Oral flucloxacillin
IV flucloxacillin if severe
Alternative for oral flucloxacillin for mild-moderate cellulitis
Oral doxycycline
Alternative for IV flucloxacillin for severe cellulitis
IV vancomycin
What is a useful thing to do to check if the cellulitis is still spreading
Mark the margins of erythema
What is impetigo
Superficial skin infection occurring at stratum corneum (immediately below the skin)
Impetigo is most common in
Children
Infants
Impetigo is most commonly caused by
S aureus
Strep pyogenes
Symptoms of impetigo
Pruritus
Well defined lesions
Golden crust lesions with erythematous base
Impetigo usually occur at
Face
Investigations for impetigo
Clinical
Swab under certain conditions
Under what conditions can you request for a skin swab for suspected impetigo
if the impetigo is
Severe
Recurrent
MRSA suspected
Management for impetigo
Topical fusidic acid
Oral flucloxacillin or clarithromycin
Avoid sharing towels
Do not attend school until completion of antibiotic treatment
Why should children with impetigo avoid sharing towels / remain good hygiene
Because impetigo is highly contagious
Difference between cellulitis and impetigo
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
What is erysipelas
Infection of the dermis and UPPER subcutaneous tissue (more superficial than cellulitis)
Most erysipelas is caused by
Streptococcus pyogenes
Risk factors for erysipelas
Venous insufficiency
Immunocompromised
Breaks in skin barriers
Fissured toes / heels
Nasopharyngeal infections
Symptoms of erysipelas
Well demarcated, raised, swollen, erythematous, firm area
Fever
Systemic upset
Distribution of erysipelas
Mostly lower limbs
Butterfly distribution over the cheeks and bridge of nose
investigations for Erysipelas
Clinical
Cultures from entry of infection
Cultures from blister fluids
imaging if bone is suspected to be involved
Management for erysipelas
Rest
Analgesia
Elevate
Antibiotics
- Oral flucloxacillin
- IV flucloxacillin if severe
Describe the antibiotics used for erysipelas
Oral flucloxacillin
IV flucloxacillin if severe
Alternative for oral flucloxacillin for erysipelas
Erythromycin
What is necrotising fasciitis
Life threatening infection of subcutaneous tissue with spread along the fascial planes but not underlying muscles
Necrotising fasciitis causes extensive necrosis of
Superficial fascia
Subcutaneous fat
There are 4 types of necrotising fasciitis. Which ones are the most common
Type 1 - polymicrobial infection
Type 2 - mono microbial infection
What is type 1 necrotising fasciitis caused by
Different anaerobes
What is type 2 necrotising fasciitis caused by
Group A streptococci
Risk factors for necrotising fasciitis
Immunocompromised
Obesity
Person who inject drugs
Injuries
Peripheral arterial disease
Symptoms of necrotising fasciitis
Systemically unwell - tachycardia / tachypnea / pyrexic / hypotensive
Rapidly spreading diffuse erythema
Blisters
Oedema
Very painful
Purple discolouration
Crepitus over site
What may be the only sign in early stage of necrotising fasciitis
Mild oedema
Investigations for necrotising fasciitis
Blood cultures
Deep tissue cultures
Management for necrotising fasciitis
Urgent surgical debridement
Broad spectrum antibiotics
How do cancer cells emerge
- Originate from a single cell
- A genetic mutation causes the rise of cancer cells
- Series of mutations accumulate in successive generations (clonal evolution)
- Cell accumulates enough mutations to become cancerous
Describe clonal evolution
- All cancer cells originate from an initiating mutation (this mutation allows it to be cancerous)
- Clonal expansion occur -> more cells with the first mutation
- Another mutation occurred during expansion. This gives survival benefits to the cancer cell
- Clones of the first and second mutations produced and outcompetes the ones with only the first mutation
- Eventually accumulate enough mutations to make it cancerous
Function of proto-oncogene
Positively regulates normal cell division (i.e. causes cell division when needed)
What is the mutated form of proto-oncogene called
Oncogene
Proto-oncogene or oncogene drives tumour formation
Oncogene
Function of tumour suppressor gene
Under certain factors, triggers:
Cell cycle arrest
Cell apoptosis
DNA repair
Blocking angiogenesis
What factors can cause p53 to stop cell division
UV radiation
Lack of nucleotides
Hypoxia
Ionising radiation
Examples of proto-oncogenes
Ras
Raf
growth factor receptors
Example of tumour suppressor gene
p53
Describe how UV radiation may lead to rise of cancer
- UV radiation causes damage to cells
- normal p53 gene in cells detect the abnormality and induces cell apoptosis
- However, one of the damaged cells already has a faulty p53 gene so it does not undergo apoptosis
- This allows the cancerous cell to proliferate (clonal expansion), accumulating more mutations
- Causes cancer
Types of UV light
UVC
UVB
UVA
Which UV light can pass through glass window
UVA
Which UV light is more damaging
UVB
Which UV light is blocked by the ozone layer
UVC
Which UV light has the longest wavelength
UVA
What can block UVA
Sunscreen
What can block UVB
Sunscreen
Window glass
Damage from UVA causes
Pigmentation
Skin cancer
Photoaging
Damage from UVB causes
Sunburn
Pigmentation
Skin cancer
Photoaging
Which UV light causes indirect DNA damage
UVA
Which UV light causes direct DNA damgage
UVB
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)
What factors causes UV light to increase risk of skin cancer
Damage to DNA
Immunosuppressive
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
What are the UVB induced DNA lesions
formation of covalent linkages between adjacent pyrimidines on the same DNA strand
What are the UVB signature mutations
CT
TT
UVB DNA lesions can be repaired by
Nucleotide excision repair (NER)
UVA DNA lesions can be repaired by
base excision repair (BER)
What are the 2 main types of skin cancer
Non-melanoma (keratinocyte skin cancer)
Melanoma
Which type of skin cancer is more likely to metastasise
Melanoma
What are the benign melanocytic lesions
Freckles (ephilides)
Actinic lentigenes
Naevi
Difference between benign and malignant melanocytic lesions
Benign ones
-well demarcated borders
-not changing rapidly
-even pigmentation
-symmetrical
What are freckles
Patchy increase in melanin after UV exposure
What causes freckles
1 defective copy of MC1R gene (which controls type of melanin produced)
Freckles are common in
fair skin
red heads
What are actinic lentigines (age / liver spots)
small, gray-brown spots common in elderly that appear due to UV exposure
Actinic lentigines are most commonly found on
face
dorsal hands
forearms
Histology of actinic lentigenes will show
epidermis with elongated rate ridges (epithelial extensions that extend to dermis)
Increase melanin and basal melanocytes
What are congenital melanocytes naevi
Visible pigmented lesions present at birth due to benign proliferation of melanocytes
Congenital melanocytic naevi type of naevus
Junctional naevus
What are junctional naevus
When melanocytes proliferate and form clusters at DEJ
What do congenital melanocytic naevi look like
flat
smooth surface
even pigmentation
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
Common acquired naevus type of naevus
Compound
What are compound naevus
Naevus due to clusters of melanocytes at epidermal junction and dermis
What are intradermal naevus
Naevus due to clusters of melanocytes at dermis
Describe the presentation of dysplastic naevi
> 6mm
Irregular border
Asymmetry
Uneven pigmentation
May be bumpy
Difference between dysplastic naevi and melanoma
Dysplastic naevi is not cancerous yet but has high chance of developing into melanoma
What is sporadic dysplastic naevi
Dysplastic naevi that is not inherited and slightly raises the risk of malignant melanoma
Patient with familial dysplastic naevi often has
family history of melanoma
Inheritance of CDKN2A
What does it mean if a patient has inherited CDKN2A gene
High risk of developing many atypical naevi throughout their whole life
Which type of dysplastic naevi increases the risk of melanoma more
Familial dysplastic naevi
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
Use of ABCDE rule for melanoma
Refer urgently if any lesions present with any of the features
ABCDE features for melanoma
Asymmetry
Border irregularity
Colour variation
Diameter >6mm
Evolution over time
What other sign can be used to identify malignant lesion
Ugly duckling sign - any lesions that doesn’t look like the others
Risk factors for melanoma
Intermittent sun burn in childhood
Increasing age
Use of sun beds
Family history
Skin type 1
Dysplastic naevi
Melanoma mostly arise from
de novo - from normal skin
only 25% arise from pre-existing naevi
On which body parts do melanoma most commonly occur on
Sun exposed sites such as
Scalp
Face
Neck
Arm
Trunk
leg
Types of melanoma
Superficial spreading
Nodular
Lentigo Maligna
Acral lentingious
What are the 2 phases of growth of melanomas (except nodular melanoma)
Radial growth
Vertical growth
Nodular melanoma only has which growth phase
Vertical growth
Describe the 2 phases of growth of melanoma (except nodular)
- Radial growth: growing horizontally as macules not nodules. May invade the papillary layer of dermis
- Vertical growth: growth vertically and invading the dermis (deeper into the tissue), forming a tumour
Which type of melanoma is the most common
Superficial spreading melanoma
Superficial spreading melanoma is most commonly seen in
Trunk
Limbs
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
Which type of melanoma is usually presented late
Acral lentingious
Where does acral lentingious melanoma usually occur
Palms
Soles of feet
What is lentigo maligna melanoma
Melanoma that arise from pre-existing lentigo maligna
Where does lentigo maligna melanoma usually occur
Face
Scalp
Neck
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
Where do melanocytes migrate from during embryo stage
Neural crest
When should you suspect a lesion may be melanoma
New pigment lesion develops in adulthood
ABCDE
Ulceration
Bleeding
Investigation for melanoma
Narrow complete excision of lesion for biopsy
Breslow depth assessment
What is Breslow depth assessment
Measures the depth of tumour to assess the prognosis
Where should you measure from for breslow depth if the lesion is ulcerated
Base of ulcer to deepest tumour cell
What should be carried out to look for metastasis if breslow depth is > 1mm
Sentinel lymph node biopsy
Stage 1 melanoma breslow depth
<1 mm
Stage 2 melanoma breslow depth
1-2 mm
Stage 3 melanoma breslow depth
3-4 mm
Stage 4 melanoma breslow depth
> 4 mm
Management of melanoma
Stage 0 - 2 : wide excision to remove all tumour cells
Stage 3, 4: chemo, immunotherapy, genetic therapies
What are the genetic therapies
Imatinib
Debrafenib/vemurafenib
What is seborrheic keratosis
Benign epidermal lesion caused by proliferation of epidermal keratinocytes
Seborrheic keratosis is more common in which age group
Elderly, ageing skin
Seborrheic keratosis commonly present on
Face
Trunk
Appearance of seborrheic keratosis
Brown
Waxy surface
Warts and depressions on surface
Slightly raised
Well demarcated
What is Leser Trelat sign
Sudden emergence of many seborrhoeic keratosis which is associated to certain cancers
Which cancers are associated to Leser Trelat sign
Adenocarcinoma of stomach / colon
Squamous cell carcinoma
Lymphoma
Leukemia
What may be seen in histology of seborrheic keratosis
Horn cysts
Acanthosis
How are seborrheic keratosis managed
nothing usually unless patient wants it to be removed
Investigate further if leser trelat sign
What are the premalignant conditions of squamous cell carcinoma
Actinic keratosis
Bowen’s disease
Premalignant conditions of SCC all causes which histological feature
Squamous dysplasia
Cause of actinic keratosis
Chronic sun exposure damaging DNA
Risk factors of actinic keratosis
Type I or II skin
History of sunburn
Outdoor occupation or hobbies
Immunosuppression
Histology presentation of actinic keratosis
Partial thickness squamous dysplasia of epidermal keratinocytes
Presentation of actinic keratosis
scaly, erythematous papules or patches
feels rough
Where do actinic keratosis occur on
Sun exposed surfaces
- scalp
- face
- dorsum of hands
Around what proportion of patients with actinic keratosis develop into SCC
< 1%
Management of small actinic keratosis
If localised - curettage / cryotherapy / surgery
Management of large actinic keratosis
5-fluorouracil
+ NSAID or imiquimod
What is Bowen’s disease
squamous cell carcinoma in situ - premalignant lesion that is confined to epidermis
Histology presentation of Bowen’s disease
Full thickness squamous dysplasia of epidermal keratinocytes
Presentation of Bowen’s disease
slowly enlarging, well-demarcated, scaly red patch/plaque with an irregular border
Bowen’s disease most commonly present on
legs in women
torso in men
A variant of Bowen’s disease affects
genital mucosa
The variant of Bowen’s disease that affects the genital mucosa is linked to which diseases
HPV
HIV
Management of Bowen’s disease
Cryotherapy
Curettage
surgery
5-fluorouracil
imiquimod / NSAID
