DERM Flashcards
(175 cards)
1
Q
ACNE VULGARIS
what are the risk factors?
A
- teenagers + young adults
- family history
- medications (corticosteroids, androgens)
2
Q
ACNE VULGARIS
Briefly describe the pathophysiology of acne
A
comedones are non-inflammatory lesions and can be open (blackheads) or closed (whiteheads). When the follicle bursts, inflammatory lesions such as papules and pustules may form. Excessive inflammation results in nodules, and cysts
3
Q
ACNE VULGARIS
Describe the signs of acne
A
MILD
- non-inflamed lesions (open + closed comedones) with few inflammatory lesions
MODERATE
- more widespread
- increased inflammatory papules + pustules
SEVERE
- widespread inflammatory papules pustules, nodules or cysts
- scarring
4
Q
ACNE VULGARIS
Describe the treatment for acne
A
1st line
- topical retinoid +/- benzoyl peroxide,
- topical antibiotic (clindamycin)
- topical azelaic acid 20%
2nd line
- oral tetracycline (doxycycline, lymecycline) with topical benzoyl peroxide +/- topical retinoid
- COCP (co-cyprindiol)
3rd line
- isotretinoin (accutane)
5
Q
ECZEMA
what are the different types?
A
- atopic dermatitis (most common)
- contact dermatitis = exposure to irritants
- dyshidrotic eczema = blistering on hands/feet
- seborrheic dermatitis
- venous dermatitis
6
Q
ECZEMA
what is the pathophysiology?
A
the presence of a defect in the epidermal barrier due to polygenic mutations, allowing for sensitisation against allergens.
An immune response is subsequently triggered following sensitisation, leading to IgE production and eosinophilia. The result is itchy, dry patches of skin.
7
Q
ECZEMA
what are the risk factors?
A
- developed world
- urban area
- atopy
- family history
- triggers - irritants (soaps/detergents), cold, dampness, dust mites, pollen
8
Q
ECZEMA
what are the clinical features?
A
- pruritus
- dry skin
- erythema
- vesicles + pustules
- lichenification (chronic disease)
- excoriations
9
Q
ECZEMA
where is it most commonly found on infants?
A
face
extensor surfaes
10
Q
ECZEMA
where is it most commonly found on children and adults?
A
flexural surfaces
11
Q
ECZEMA
what are the investigations?
A
- clinical diagnosis
- allergy testing if specific allergy is suspected
12
Q
ECZEMA
what is the management?
A
MILD
- emollients
- mild corticosteroids (hydrocortisone 1%)
MODERATE
- emollients
- moderate corticosteroids (betamethasone 0.025% or clobetasone 0.05%)
- antihistamines
SEVERE
- emollients
- potent corticosteroid (betamethasone 0.1%)
- oral corticosteroid
- antihistamine
13
Q
BCC
what is the pathophysiology?
A
arises from basal cells
sun exposure leads to UV-related DNA damage
slow growing - mets are rare
14
Q
BCC
what are the risk factors for BCC?
A
- male
- UV exposure
- fair skin
- xeroderma pigmentosa
- immunosuppression
- arsenic exposure
15
Q
BCC
where is it most commonly found?
A
face, neck, ears and chest
16
Q
BCC
what is the clinical presentation?
A
- pearly indurated flesh-coloured papule with rolled border
- covered in telangiectasia
- may ulcerate + create central crater
17
Q
BCC
what are the investigations?
A
- referral to dermatology
- usually a clinical diagnosis
- biopsy if unsure (nodules of basal cells + palisading)
18
Q
BCC
what is the management?
A
1st line
- surgery (excision or curettage & cautery)
other options
- radiotherapy
- cryotherapy or topical therapy (imiquimod and fluorouracil)
19
Q
BCC
what is the prognosis?
A
very good - rare for it to metastasise
20
Q
CELLULITIS
what is it?
A
infection of the dermis and subcutaneous tissue
21
Q
CELLULITIS
what are the most common causes?
A
- s.aureus
- s.pyogenes
22
Q
CELLULITIS
what are the risk factors?
A
- break in cutaneous barrier
- immunocompromise
- other skin conditions (eczema, shingles)
- history of cellulitis
- obesity
- venous insufficiency
- lymphoedema
23
Q
CELLULITIS
what are the clinical features?
A
- red, hot and painful area
- fever
- macular erythema with indistinct borders
- shiny skin
- oedema
24
Q
CELLULITIS
what are the investigations?
A
FBC + CRP
swab
25
CELLULITIS
how is it classified?
Erons classification
CLASS 1 - no systemic signs (outpatient/oral abx)
CLASS 2 - systemically unwell or systemically well but have comorbidity (possible admission)
CLASS 3 - significant systemic upset (admission required)
CLASS 4 - sepsis
26
CELLULITIS
what is the management?
antibiotics
- 1st line = flucloxacillin
- if penicillin allergic = clarthromycin/erythromycin/doxycycline
- 1st line if near eyes/nose = co-amoxiclav
- severe infection = co-amoxiclav/cefuroxime/clindamycin
- MRSA = add vancomycin
27
CONTACT DERMATITIS
what is it?
skin reaction to external agent
can be irritant or allergic
28
CONTACT DERMATITIS
what is the pathophysiology?
irritant = direct toxicity by an agent
allergic = delayed hypersensitivity reaction (requires prior sensitisation)
29
CONTACT DERMATITIS
what are the different types?
irritant contact dermatitis (ICD)
allergic contact dermatitis (ACD)
30
CONTACT DERMATITIS
give some examples of common allergens that cause contact dermatitis
nickel sulfate
neomycin
formaldehyde
sodium gold thiosulfate
31
CONTACT DERMATITIS
what are the risk factors?
- occupation with frequent exposure to water and caustic materials e.g. labourers, chefs, farmers
- history of atopic eczema
32
CONTACT DERMATITIS
what are the clinical features?
- erythema
- pruritus (more common in ACD)
- burning (more common in ICD)
- vesicles (more common in ACD)
- affects hands and face
- sparing of non-exposed areas
33
CONTACT DERMATITIS
what are the clinical features of chronic contact dermatitis?
scaling
lichenification
34
CONTACT DERMATITIS
how long do symptoms last for?
- ICD takes 3-6 weeks to resolve
- ACD typically resolves within a few days
35
CONTACT DERMATITIS
what are the investigations?
- skin patch testing
- repeated open application test
can consider skin biopsy
36
CONTACT DERMATITIS
what is the management for irritant contact dermatitis (ICD)?
1st line
- avoidance of irritant
- skin emollients
2nd line
- topical corticosteroids (hydrocortisone, betamethasone)
37
CONTACT DERMATITIS
what is the management of allergic contact dermatitis (ACD)?
1st line
- avoidance of allergen
- topical corticosteroids (hydrocortisone, betamethasone)
2nd line
- topical calcineurin inhibitors (tacrolimus, pimecrolimus)
3rd line
- oral corticosteroids (prednisolone, dexamethasone)
- phototherapy (BUVB, PUVA)
- immunosuppressants (azathioprine, ciclosporin)
38
CUTANEOUS WARTS
what are they?
benign skin growths typically caused by human papillomavirus (HPV) types 2 and 4
39
CUTANEOUS WARTS
what is the pathophysiology?
they are caused by human papillomavirus (HPV) types 2 and 4
The virus invades the skin through small cuts or abrasions and causes rapid growth of cells on the outer layer of the skin, leading to the formation of a wart
40
CUTANEOUS WARTS
what are the different types of warts?
- common warts (verruca vulgaris) = papular with irregular border, seen at extremities
- plantar warts (verruca plantaris) = only occur on feet
- flat warts (verruca plana)
- filiform warts
41
CUTANEOUS WARTS
what are the risk factors?
- use of public showers
- close contact with a person with warts
- skin trauma
- immunosuppression
- meat handlers
- Caucasian ethnicity
42
CUTANEOUS WARTS
what are the clinical features?
often asymptomatic
- firm rough papules or nodules
- interrupted skin lines over warts
- black dots within wart (thrombosed capillaries)
43
CUTANEOUS WARTS
what are the investigations?
typically clinical diagnosis
can do biopsy
44
CUTANEOUS WARTS
what is the management?
1st line
- watchful waiting
- topical salicylic acid
2nd line
- cryotherapy (freezing with liquid nitrogen)
- immunotherapy
45
CUTANEOUS WARTS
what are the complications?
- spread of warts to other areas of the body or other people
- pain or discomfort
- scarring or changes to skin
- transformation to SCC (very rare, in immunocompromised)
46
FOLLICULITIS
what is it?
inflammation of the hair follicle
can be infectious (viral, bacterial or fungal) or non-infectious
47
FOLLICULITIS
what is the most common causative organism?
s.aureus
48
FOLLICULITIS
what are the risk factors?
- trauma (shaving, hair extraction)
- topical corticosteroid use
- diabetes mellitus
- immunosuppression
- drug-induced (corticosteroids, androgenic hormones, isoniazid, lithium)
- hot tub use
chronic inflammatory skin disease
49
FOLLICULITIS
what is hot tub folliculitis caused by?
pseudomonas aeruginosa
50
FOLLICULITIS
what are the clinical features?
SYMPTOMS
- erythema
- papules (small, clusters)
- pustules (small, whiteheads)
- pruritis (localised)
SIGNS
- localised to shaving area
- blistering if severe
- subdermal mass (abscess if severe)
- raised eosinophils
51
FOLLICULITIS
what are the investigations?
uncomplicated can be diagnosed via appearance
to consider
- bacterial skin swab
- viral skin swab
- skin scraping
- skin biopsy
52
FOLLICULITIS
what is the management?
CONSERVATIVE
- use clean sterile razors for shaving
- wear loose clothing
- antibacterial soap
- avoid hot tubs
MEDICAL
- mild = no treatment or topical antibiotics
- moderate bacterial = oral flucloxacillin (s.aureus) or oral ciprofloxacin (pseudomonas)
- moderate viral = oral aciclovir
- moderate fungal = ketoconazole, fluconazole, itraconazole
53
CUTANEOUS FUNGAL INFECTION (RINGWORM)
what is it?
superficial fungal infection of keratinised tissue (skin, hair, nails) caused by a group of fungi known as dermatophytes
54
CUTANEOUS FUNGAL INFECTION (RINGWORM)
what are the different types?
Tinea pedis: feet involvement, also known as athlete’s foot
Tinea corporis: truncal involvement
Tinea capitis: scalp involvement
Tinea cruris: groin involvement
Tinea unguium: fungal nail involvement
55
CUTANEOUS FUNGAL INFECTION (RINGWORM)
what are the risk factors?
- close contact with infected individuals or animals
- damp, warm environments
- participation in contact sports
- shared facilities
- immunocompromised states
56
CUTANEOUS FUNGAL INFECTION (RINGWORM)
what are the clinical features?
SYMPTOMS
- itching
- discomfort
- hair loss
SIGNS
- annular (ring shaped lesions)
- central clearing of the rash
- scaling of the skin
- erythema
- nail thickening and crumbling
57
CUTANEOUS FUNGAL INFECTION (RINGWORM)
what are the investigations?
- clinical diagnosis
to consider
- microscopy and culture
- woods lamp examination
58
CUTANEOUS FUNGAL INFECTION (RINGWORM)
what is the management?
1st line
- topical antifungals (clomitrazole, terbinafine)
- skin care (avoid sharing towels, keep area clean and dry)
2nd line
- oral antifungals (terbinafine, itraconazole, fluconazole)
59
HEAD LICE
what causes head lice?
parasites (Pediculus humanus capitis) cause an infestation called pediculosis capitis
60
HEAD LICE
what is the lifecycle of head lice?
Firstly, louse eggs are laid on the scalp and are grey or brown in colour
Then these eggs hatch in 7-10 days releasing baby lice (nymphs); the empty shells are referred to as “nits” and are visible as white and shiny shells
Finally, nymphs take another 7-10 days to mature into adult head lice
Adult head lice cling to hair roots via claws on their 6 legs
Female lice will lay 50-150 eggs during their 30-40 day lifespan
61
HEAD LICE
how is it transmitted?
direct head-to-head contact
cannot swim, fly or jump
are not transmitted by pets
62
HEAD LICE
what are the risk factors?
- young age
- female (more likely to have longer hair)
- long hair
- siblings with head lice
- low socioeconomic status
63
HEAD LICE
what are the clinical features?
SYMPTOMS
- itchy scalp
- feeling something moving in hair
SIGNS
- oval-shaped white eggs on scalp
- brown insects on scalp
- excoriation marks on scalp, neck and behind ears
64
HEAD LICE
what are the investigations?
active infestation = live head louse found
all household members should be investigated
- detection combing
- visible inspection
65
HEAD LICE
what is the management?
1st line
- medicated lotions/sprays (dimeticone, isopropyl myrisate, cyclomethicone)
- wet combing (over 2 week period, days 1, 5, 9 and 13)
- insecticide (malathion)
66
HEAD LICE
what is the general advice?
- all affected household members should be treated on the same day
- children being treated can still attend school
- no need to hot-wash clothes
- only treated if live lice are found
67
IMPETIGO
what is it?
superficial bacterial skin infection usually caused by the gram-positive bacteria Staphylococcus aureus or Streptococcus pyogenes
68
IMPETIGO
what are the different types?
non-bullous (most common)
bullous
69
IMPETIGO
what is the pathophysiology?
The bacteria invade the superficial layers of the epidermis leading to macule formation . Once a lesion is present, self-inoculation to other sites is common .
Non-bullous impetigo = the lesion will develop into a vesicle or pustule and coalesce before rupturing. Once ruptured, the exudate forms a characteristic honey-coloured crust with an erythematous base .
Bullous impetigo = vesicles appear and become flaccid bullae before rupturing
70
IMPETIGO
what is primary vs secondary impetigo?
primary = occurs in previously normal skin by direct bacterial invasion
secondary = infected wound site affected by another condition
71
IMPETIGO
what are the most common causative organisms?
s.aureus = most common
s.pyogenes
72
IMPETIGO
what are the risk factors?
- younger age
- close contact with infected people
- other skin conditions e.g. eczema
- environmental factors (increased humidity, poor hygiene)
73
IMPETIGO
what are the clinical features of non-bullous impetigo?
- honey crusted lesions after vesicles have ruptured
- lesions occur anywhere on the body (most likely face/chin)
74
IMPETIGO
what are the clinical features of bullous impetigo?
- vesicles become flaccid, fluid-filled bullae
- rupture after 2-3 days leaving flat honey crusted lesion
- systemic features e.g. fever, diarrhoea + lymphadenopathy
75
IMPETIGO
what are the investigations?
clinical diagnosis
to consider
- swab
76
IMPETIGO
what is the management?
non-bullous
- localised = hydrogen peroxide 1% cream or topical antibiotic (fusidic acid, mupirocin)
- widespread = topical (fusidic acid or mupirocin) or oral antibiotics (flucloxacillin, clarithromycin or erythromycin)
bullous
- oral antibiotics (flucloxacillin, clarithromycin or erythromycin)
77
IMPETIGO
what is the general advice for school/work?
- avoid sharing towels
- stay away until lesions have healed, dry and crusted over or 48 hours after initiation of antibiotics
78
LICHEN PLANUS
what is it?
inflammatory condition of the skin and mucous membranes
‘Lichen’ means small bumps on the skin and ‘planus’ means flat, providing a description of the rashes appearance
79
LICHEN PLANUS
what is the pathophysiology?
immune response leading to T-cell mediated inflammation and keratinocyte apoptosis
80
LICHEN PLANUS
what are the different types?
classified based on site affected
- cutaneous lichen planus
- oral lichen planus
- lichen planus of nails
- lichen planopilaris (scalp)
- genital lichen planus
81
LICHEN PLANUS
what are the risk factors?
- ages 40-60
- hep C
- drugs (thiazide diuretics, beta-blockers, NSAIDS and antimalarials)
- vaccinations
- stress
- family history
82
LICHEN PLANUS
what are the clinical features?
SYMPTOMS
- itching
- oral discomfort
- hair loss
SIGNS
- purple, polygonal, flat-topped papules on wrists, ankles and lower back
- wickhams striae (white streaks overlying rash)
- rough thinning nails with grooves
- sore, red patches on vulva
- ring-shaped (annular) purple/white patches on penis
83
LICHEN PLANUS
what are the investigations?
clinical diagnosis
to consider
- skin biopsy
- hep c testing
84
LICHEN PLANUS
what is the management?
1st line
- topical corticosteroids
- conservative (wash with warm water, emollients, avoid tight clothing)
2nd line
- oral corticosteroids
- topical calcineurin inhibitors (tacrolimus)
- phototherapy
85
MALIGNANT MELANOMA
what is it?
a malignant tumour arising from the melanocytes in the skin
86
MALIGNANT MELANOMA
where can it affect?
- previously healthy skin (de novo)
- existing precursor lesion
- GI tract
- brain
87
MALIGNANT MELANOMA
why can it affect GI tract and brain?
melanocytes are derived from neural crests
melanoma can occur anywhere neural cells migrate such as GI tract and brain
88
MALIGNANT MELANOMA
what are the growth phases of melanomas? which is more dangerous?
radial = growth of malignant cells in the epidermis
vertical = growth of malignant cells into dermis (more likely to lead to metastasis and poorer prognosis)
89
MALIGNANT MELANOMA
what is the most common gene mutation associated with melanomas?
BRAF gene mutation - found in 50% of cases
90
MALIGNANT MELANOMA
what are the risk factors?
- increasing age
- family history
- pale skin (fitzpatrick type I and II)
- red/blonde/light coloured hair
- UV exposure
- precursor lesions (dysplastic naevi)
- previous skin cancer
- immunosuppression
- xeroderma pigementosum
91
MALIGNANT MELANOMA
how do you assess a nevus?
ABCDE
A - asymmetry of lesion
B - border irregular
C - colour non-uniform
D - diameter >6 mm
E - evolution: changing shape, size or colour
92
MALIGNANT MELANOMA
what are the different types?
- superficial spreading (most common, horizontal growth)
- nodular (may ulcerate + bleed, vertical growth)
- lentigo maligna (seen in elderly, on face)
- acral lentiginous (palms, soles and nailbed, more common in darker skin)
- amelanotic (pink, lack pigment)
93
MALIGNANT MELANOMA
what is the diagnostic criteria?
MAJOR (2 points each)
- change in size
- irregular shape/border
- irregular colour
MINOR (1 point each)
- largest diameter >7mm
- inflammation
- oozing or crusting
- change in sensation (including itch)
>3 points = strong concerns about cancer
94
MALIGNANT MELANOMA
what are the investigations?
- dermoscopy (ABCDE)
- excision biopsy
to consider
- sentinel node biopsy
- CT chest, abdomen and pelvis
- genetic studies
95
MALIGNANT MELANOMA
how is it staged?
AJCC staging system
0 = confined to epidermis, melanoma in situ
1 = breslow thickness <2mm, no nodal involvement/mets
2 = breslow thickness 1-2mm with ulceration, or >2mm with/without ulceration, no nodal involvement/mets
3 = any thickness, involvement of local skin/LN
4 = any thickness, distant mets/LN
96
MALIGNANT MELANOMA
what is the management?
EARLY STAGE (0-2)
- excision with adequate margin
- topical imiquimod
STAGE 3
- LN dissection
- radiotherapy
- resection of mets
STAGE 4
- systemic treatments (chemo/immunotherapy)
- radiotherapy
- resection of mets
97
MALIGNANT MELANOMA
where does it tend to spread to?
lymph nodes
brain
bones
liver
lung
GI tract
98
MALIGNANT MELANOMA
what is the most important indicator of prognosis?
Breslow thickness = depth of extension into the dermis
99
PITYRIASIS ROSEA
what is it?
inflammatory skin condition of uncertain aetiology, though an association with human herpesviruses 6 and 7
100
PITYRIASIS ROSEA
what is the characteristic feature?
herald patch - single, oval scaly patch up to 10cm diameter and appears 2 weeks before rest of rash
101
PITYRIASIS ROSEA
what are the investigations?
clinical diagnosis
102
PITYRIASIS ROSEA
what are the clinical features?
- herald patch
- itchy rash (erythematous, oval, papular scaly patches on trunk + extremities)
- fir tree appearance
103
PITYRIASIS ROSEA
what is the management?
- emollients
- topical steroid = mild (hydrocortisone 1%) or moderate (betamethasone valerate 0.025%)
- antihistamine (chlorphenamine) if itching affects sleep
104
PITYRIASIS VERSICOLOR
what is it?
common superficial fungal infection caused by the Malassezia species, a yeast that is part of the normal skin flora
105
PITYRIASIS VERSICOLOR
what are the risk factors?
- hot and humid climates
- excessive sweating
- oily skin
- immunocompromised
- age (teenagers + young adults)
106
PITYRIASIS VERSICOLOR
what are the clinical features?
- itching (may also be asymptomatic)
- rash on back, chest and upper arms
- well-demarcated round/oval scaly patches
- rash worsens with sun exposure
- colour variation
107
PITYRIASIS VERSICOLOR
what are the investigations?
clinical diagnosis
to consider
- woods lamp exam
- microscopy of skin scrapings
108
PITYRIASIS VERSICOLOR
what is the management?
1st line
- topical antifungals (ketonazole, selenium sulphide shampoo)
- sun protection
2nd line
- oral antifungals (fluconazole)
109
PSORIASIS
what is it?
chronic, systemic, inflammatory skin disease with a multifactorial aetiology
110
PSORIASIS
what is the pathophysiology?
- immune-mediated
- abnormal T-cell activity that stimulates proliferation of keratinocytes
111
PSORIASIS
what are the genetic factors that are strongly associated with psoriasis?
HLA-B13
HLA-B17
112
PSORIASIS
what are the risk factors?
- family history
- obesity
- smoking and alcohol consumption
- medications (ACEi, BB, NSAIDs, lithium, hydroxychloroquine, steroid withdrawal, abx)
113
PSORIASIS
what are the clinical features?
- skin plaques (well-demarcated, scaly, on extensor surfaces)
- pruritus
- nail changes (pitting, onycholysis, subungual hyperkeratosis, nail loss)
114
PSORIASIS
what are the nail changes?
- pitting
- onycholysis
- subungual hyperkeratosis
- nail loss
115
PSORIASIS
what are the different types?
- chronic plaque (most common)
- scalp psoriasis
- facial psoriasis
- flexural psoriasis
- localised pustular psoriasis
- guttate psoriasis (widespread teardrop, triggered by strep infection)
- erythrodermic psoriasis (medical emergency)
116
PSORIASIS
what are the investigations?
- clinical diagnosis
117
PSORIASIS
what is the management?
1st line
- patient education
- regular emollients
- topical corticosteroids + vit D for 4 weeks
- if poor response, continue for 4 more weeks
- if poor response after 8 weeks, stop corticosteroid + take vit D BD
- if poor response after 12 weeks, potent topical steroid BD for 4 weeks
2nd line
- short-acting dithranol
- phototherapy
3rd line
- DMARDS (methotrexate, apremilast, ciclosporin)
- biologics (adalimumab, infliximab)
118
PSORIASIS
what are the complications?
- psoriatic arthropathy
- mood disturbance
- cardiovascular disease
- venous thromboembolism
119
SCABIES
what is it?
is an intensely itchy skin infestation caused by the human parasitic mite, Sarcoptes scabiei.
Scabies mites burrow into the epidermis, laying their eggs in the stratum corneum
120
SCABIES
what is the pathophysiology?
- infestation with Sarcoptes scabiei
- type IV hypersensitivity reaction
121
SCABIES
how are they transmitted?
- direct skin-to-skin contact for a prolonged period of time
- can be transmitted through bedding and clothing
122
SCABIES
what are the risk factors?
- sub-tropical and developing countries
- crowded conditions
- adolescence
- female sex
- winter months
123
SCABIES
how long does it take for symptoms to develop?
- 1st time exposure = 3-6 weeks
- it is contagious before the rash develops
- in cases of re-infestation = 1-3 days
124
SCABIES
what are the clinical features?
SYMPTOMS
- intense pruritus (particularly at night)
- symmetrical erythematous papules (on wrists and between fingers)
SIGNS
- excoriation marks
- linear crooked burrows (sides of fingers + flexor wrist)
125
SCABIES
what are the investigations?
- clinical history/exam (new sexual contacts, overcrowded living, household members)
to consider
- ink burrow test
- skin scraping
- immunodeficiency screen
126
SCABIES
what is the management?
1st line
- permethrin 5% cream
- topical crotamiton cream (symptomatic relief)
2nd line
- malathion aqueous 0.5%
127
SCABIES
what is the general advice?
- avoid having sex or physical contact until completion of full treatment course
- avoid sharing bed or clothing
- bedding, clothing and towels should be washed at 60 degrees and dried in hot dryer on first day of treatment
128
SCC
what is it?
skin cancer arising from squamous cells in epidermis
129
SCC
what is the pathophysiology?
cumulative sun exposure and UV radiation
causes DNA damage and genetic mutations resulting in uncontrolled cell growth
130
SCC
what is the pre-cancerous form of SCC?
actinic keratosis
131
SCC
what are the invasive forms of SCC?
- cutaneous horn
- marjolin ulcer
- keratoacanthoma
132
SCC
what is the epidemiology?
accounts for 20% of skin cancers (2nd most common)
more common with fair skin, light hair and light eye colour
133
SCC
what are the risk factors?
- sun exposure and history of sunburns
- use of tanning beds
- chronic skin inflammation or injury
- HPV infection
- immunosuppression
134
SCC
what are the clinical features?
SYMPTOMS
- itchy, tender or painful lesions
- ulcerating lesions
- lesions on sun-exposed areas
SIGNS
- scaly or erythematous lesions
- crusted or indurated lesions
- bleeding lesions
- irregular borders
135
SCC
what are the investigations?
- dermscopy
- skin biopsy
to consider
- CT TAP
136
SCC
what is the management?
- surgical excision (wide local or Mohs)
- agressive cryotherapy
- topical 5-fluorouracil
- imiquimod
- radiotherapy
137
SCC
what is the prognosis?
- generally good (5 year cure rate = 95%)
138
NECROTISING FASCIITIS
what is it?
a rare and life-threatening bacterial infection characterised by rapidly spreading necrosis of the fascia and subcutaneous tissues, including muscles and skin
139
NECROTISING FASCIITIS
what is the pathophysiology?
It arises if bacteria penetrate deep tissue via an injury (e.g. cuts, puncture wounds, bites or surgical wounds) or the bloodstream. Streptococcus pyogenes is the most common cause
140
NECROTISING FASCIITIS
what are the different types?
it is classified according to causative organism
type 1 = polymicrobial (most common)
type 2 = group A haemolytic strep (s.pyogenes)
type 3 = gas gangrene
type 4 = fungal
141
NECROTISING FASCIITIS
what are the risk factors?
- recent trauma, burns or skin infection
- increasing age
- immunosuppressed
- DM
- SGLT-2 inhibitors
- marine exposure
- close contact with someone with necrotising fasciitis
142
NECROTISING FASCIITIS
what are the clinical features?
EARLY
- intense pain
- skin puncture or injury
- flu-like symptoms
- erythema, warmness, swelling, tenderness
- hypersensitive site
- fever
LATE
- gas or crepitus
- skin necrosis
- fever
- purple/blue skin discolouration
- reduced sensation
- hypotension + tachycardia
143
NECROTISING FASCIITIS
what are the investigations?
Bloods
- FBC - raised WCC
- CRP elevated
imaging
- CT/MRI or USS
144
NECROTISING FASCIITIS
what is the management?
- immediate surgical debridement
- IV antibiotics (broad-spectrum)
- supportive care
- amputation
145
NECROTISING FASCIITIS
what are the complications?
- fourniers gangrene
- sepsis
- death
- long-term disability
146
VIRAL EXANTHEMA
what is it?
Viral exanthema is a widespread rash that is most commonly caused by a paediatric response to systemic viral infection
147
UTRICARIA AND ANGIOEDEMA
what is urticaria?
commonly referred to as hives
characterised by rapid development of pruritic, erythematous raised wheals which vary in shape + size
148
URTICARIA AND ANGIOEDEMA
what is angioedema?
It is a swelling deep in the skin which occurs in a minority of people with urticaria or sometimes on its own.
It frequently involves the eyelids, lips and sometimes the mouth.
Sometimes the swelling can be very obvious making it difficult to open the eyes for example.
149
UTRICARIA AND ANGIOEDEMA
what is the pathophysiology?
Mast cells release histamine in response to a perceived irritant
150
URTICARIA AND ANGIOEDEMA
what are the risk factors?
- allergens (food, medications, insect stings)
- physical stimuli (pressure, cold, heat)
- infections (viral, bacterial)
- autoimmune processes
- stress + emotional factors
151
URTICARIA AND ANGIOEDEMA
what are the causes?
- viral infection
- idiopathic
- cold
- heat
- exercise
- stress
- medications - NSAIDS, antihypertensives
- thyroid function
152
URTICARIA AND ANGIOEDEMA
what are the clinical features?
- itching
- erythematous wheals with well-defined borders
- wheals vary in shape + size
- rapid onset + resolution (usually within 24hrs)
153
URTICARIA AND ANGIOEDEMA
is it an allergy?
- single episode could be allergy but there needs to be an obvious link and occur within one hour of food consumption
- most of the time it is not an allergy
154
URTICARIA AND ANGIOEDEMA
how long does it last for?
- single episode can last a few days
- can get several episodes over a 4-6 week period = viral
- recurrent angioedema + urticaria can last for 16-18 months
155
URTICARIA AND ANGIOEDEMA
what are the investigations?
clinical diagnosis
- allergy testing (skin or patch testing)
- blood tests (FBC, LFTs, TFTs, ESR and CRP)
- urinalysis
- skin biopsy
symptom diaries
severity is assessed using UAS7
156
URTICARIA AND ANGIOEDEMA
what is the management?
- 1st line = non-sedating antihistamines (cetirizine, loratadine and fexofenadine)
- 2nd line = leukotriene receptor antagonists - montelukast, or omalizumab
if symptoms persist a short course of oral corticosteroid can be used in addition to above
SYMPTOMATIC RELIEF
- calamine lotion
- topical menthol 1% aqueous cream
- sedating antihistamines (chlorphenamine) if disturbing sleep
157
GANGRENE
what are the different types?
wet gangrene = infectious gangrene (necrotising fasciitis, gas gangrene)
dry gangrene = ischaemic gangrene secondary to reduced blood flow
158
GANGRENE
what are the causes of dry gangrene?
atherosclerosis
peripheral artery disease
thrombosis
vasculitis
vasospasm
159
GANGRENE
what is the cause of gas gangrene?
clostridium perfringens
160
GANGRENE
what are the clinical features of dry gangrene?
well-demarcated necrotic area without signs of infection
161
GANGRENE
what are the clinical features of wet gangrene?
necrotic area is poorly demarcated from surrounding tissue
patients present with fever + sepsis
162
GANGRENE
what are the clinical features of gas gangrene?
- acute onset severe localised pain
- minimal local inflammation
- skin darkening + spreading erythema
- fever (hot to touch)
- gas production in affected area
- distinctive potent smell from infected area
163
GANGRENE
what are the investigations for wet gangrene?
BLOODS
- FBC
- blood cultures
- inflammatory markers (CRP + ESR)
IMAGING
- X-ray, USS or CT scan (to assess extent of disease)
TISSUE BIOPSY
- to identify causative organism
164
GANGRENE
what are the investigations for dry gangrene?
BLOODS
- FBC
- inflammatory markers (CRP + ESR)
- glucose level
- coagulation profile
IMAGING
- doppler USS or angiography
TISSUE BIOPSY
- not typically needed
165
GANGRENE
what is the management of wet gangrene?
- surgical debridement
- amputation
- broad-spectrum antibiotics
166
GANGRENE
what is the management of dry gangrene?
- surgical debridement
- amputation
167
ONYCHOMYCOSIS
what is it?
fungal nail infection - typically affects toe nails more than finger nails
168
ONYCHOMYCOSIS
what are the causative organisms?
- dermatophytes (trichophyton rubrum) = most common
- yeasts (candida)
- non-dermatophyte moulds
169
ONYCHOMYCOSIS
what are the risk factors?
- increasing age
- diabetes mellitus
- psoriasis
- repeated nail trauma
170
ONYCHOMYCOSIS
what are the clinical features?
- unsightly nails
- thickened, rough, opaque nails
171
ONYCHOMYCOSIS
what are the investigations?
nail clipping +/- scrapings
- microscopy + culture
- repeat samples may be required as false-negative rate is 30%
172
ONYCHOMYCOSIS
what is the management?
- asymptomatic = not treatment
limited involvement (<50% nail affected, <2 nails affected, superficial)
- 1st line = topical amorolfine 5% nail lacquer, 6m for hands + 9-12m for feet
extensive dermatophyte infection
- 1st line = oral terbinafine, 6w-3m for hands + 3-6m for feet
extensive candida infection
- 1st line = oral itraconazole, 'pulsed' weekly therapy
173
ROSACEA
what are the clinical features?
- typically affects nose, cheeks + forehead
- flushing is often 1st symptom
- telangiectasia
- later develops into persistent erythema with papules + pustules
- rhinophyma
- ocular involvement (blepharitis)
- sunlight may exacerbate symptoms
174
ROSACEA
what are the investigations?
clinical
175
ROSACEA
what is the management?
CONSERVATIVE
- high factor sun cream
- camouflage cream to conceal redness
SYMPTOM CONTROL
- flushing = topical brimonidine gel or oral propranolol
- telangiectasia = laser therapy
- papules/pustules
- mild-moderate = 1st line - ivermectin (other options = topical metronidazole, topical azelaic acid)
- mod-severe = topical ivermectin + oral doxycycline
