derm top tier Flashcards
acne treatment
Advice
- Avoid over washing
- Don’t pick
- Healthy diet
Mild
- Benzoyl peroxide
- – Increases skin turnover
- – Clears pores and reduces bacteria count
- – Dry
- Retinoid (tretinoin)
- – Topical
- – Inhibit formation and reduce microcomedomes
- Antibiotics
- – Topical
Moderate
- Antibiotics
- – Doxycline
- – Minocycline
- Combined oral contraceptive
- – Hormones suppress sebum production
Severe
- Retinoid (isotretinoin)
- –Decreases sebum production
acne investigations
Clinical
Skin swabs - microscopy and culture
Hormonal tests
acne complications
scarring
psychological / social
what is a comedom
in hair follicle but hair not there, instead dead skin and bacteria
open = black head closed = whitehead (skin)
acne symptoms
- different severities
Mild
- Blackheads = open comedones
- Whiteheads = closed comedones
- No scarring
moderate
- Papules - small red bumps
- Pustules - white/yellow spots
- No scarring
Moderately severe
- Inflammatory papules
- Some scarring
Severe
- Nodules - large red bumps
- Severe scarring
acne pathophysiology
- Chronic
- Hypercornification = corneodesmosomes block entrance to hair follicles, resulting in narrowing of the hair follicle
- Causes increased sebum production → greasy skin
- Sebum becomes trapped in narrow hair follicles. Stagnates at bottom of pit - it is anaerobic here, allowing propionibacterium acnes bacteria to multiply in stagnant sebum
- This results in irritation and inflammation (neutrophils attracted), so pus is formed and further inflammation
what emotion may worsen/ trigger/ cause acne
inc pathophysiology
Psychological stress → increased cortisol → increased sebum
is acne vulgaris a particularly severe form of acne?
no. vulgaris means common. this is the medical term for acne
complications of eczema
Broken skin may become infected (secondarily)
- Staph aureus
- –Crusted
- –Weeping
- Herpes simplex
- –Multiple small blisters
Depression, anxiety
treatments for more severe/ non responsive eczema
- Oral immune -modulators (cyclosporine, azathioprine)
- Oral steroids (prednisolone)
- Antibiotics (flucloxacillin)
- Phototherapy - UV A
- Antihistamines (chlorphenamine) –No clinical effect, but they sedate patient for better rest
first and second line pharmacological treatment for eczema
First line =Topical corticosteroids (hydrocortisone, clobetasol)
- Different levels for different severities
- Inhibit proinflammatory cytokines
Second line = topical calcineurin inhibitors (pimecrolimus, tacrolimus)
- Less effective but less side effects - may be good for especially sensitive areas
- calcineurin induces transcription factors for interleukins which activate T helper cells and cytokine production. so this medicine inhibits this so reduces inflammation
non pharmacological management of eczema
Hydration
- Inc emollients – artificially restore skin barrier, traps moisture
bandages
Minimising exposure to allergens
- Bath soap substitutes
Minimizing itching
eczema investigations
Clinical Bloods -- High serum IgE Must have itchy skin in past 6 months Patch testing- identifies suspected allergens Skin prick test
where is eczema often (on the body)
Elbows Knees Ankles Wrist Neck Cheeks in infants - before spreading to rest of body
describe eczema appearance
Red Itchy Scaly hyper/hypopigmented Dry Weeping/ exudation/ vesicles - if very acute
what conditions is eczema sometimes associated with
atopic triad =
Asthma
Allergic rhinitis
atopic dermatitis
Depression
Anxiety
dermatitis vs eczema
same thing
eczema pathophysiology
- Inflammatory skin disease with vesicles (when acute), redness, oedema, oozing, scaling and usually pruritus (itch)
- Skin breakdown due to stratum corneum thinning - so increased risk of inflammation
- Filaggrin is a skin barrier protein. It is damaged allowing allergens to invade more easily and hence inflammation more likely
eczema exacerbated by…
Chemicals Detergents Woolen clothes Infection Sweat Scratching / rubbing cats/ dogs Cigarette smoke Stress Weather changes
is eczema more common in children or adults
children
but common in both
types of eczema
causes/ risk factors
Endogenous - atopic
- Hypersensitivity
- Asthma , food allergy
Exogenous
- Precipitated by chemicals, sweat and abrasives over a period of time
- Sensitization of T lymphocytes
- Itching and dermatitis upon re-exposure to antigen
family history also a risk factor/ cause – faulty gene that codes for filaggrin (skin barrier protein)
psoriasis managment
advice
1st, 2nd, 3 rd line
Advice
- Avoid irritants
- Emollients
First line= topical therapy
- Vitamin D analogues (calcitriol)
- Corticosteroids
- Retinoids (vit A agonist) (tazarotene)
Second line
- Photherapy with UV A (induces damage in keratinocytes)
- DMARD (methotrexate) (+ folic acid supplements)
Third line = biologics
- TNF alpha inhibitors
- Monoclonal antibodies
Erythrodermic and pustular psoriasis presentation
Most severe
Widespread inflammation
Extremely itchy fire red scales that may fall off
Malaise, pyrexia, circulatory disturbances
palmoplantar psoriasis presentation
Red, tender, thickening of palms and soles
guttate psoriasis presentation
and age
Generalised, concentrating on trunk and upper arms/legs
Explosive eruption of very small circular/ oval (raindrop-like) plaques
Following streptococcal sore throat
children and young adults
flexural psoriasis presentation
and age
Well demarcated red, glazed plaques.
No scaling
Confined to flexures - groin, natal cleft, submammary (underboob)
later in life
chronic plaque psoriasis presentation
Most common
Well demarcated disc shaped, salmon pink silvery plaques
Thickened
Scalp common, hair margin, elbows, knees, limbs or at skin trauma sites
general psoriasis symtpoms
where
skin
nail
Where?
- Lower back
- Scalp
- Elbows
- Knees
Skin
- Thickening
- Itchy
- Painful
- Red
- Scaly
Nail changes
- Pitting (dents)
- Onycholysis (separation of nail from bed)
- Yellow-brown discolouration
- Thickening
psoriasis pathophysiology
Chronic
T lymphocyte driven hyperproliferation of keratinocytes → thickened plaques (opposite of eczema which has skin breakdown)
Inflammatory cell infiltration
psoriasis risk factors
Polygenic- family history Group a strep infection Drugs eg lithium UV light High alcohol consumption Stress
psoriasis epidemiology
gender
age
– inc age for guttate and flexural psoriasis
m=f
rare in children
Peak in early adulthood. Second less big peak 50-60y
Guttate psoriasis - children and young adults
Flexural psoriasis - later in life
risk factors for
Squamous cell carcinoma (SCC)
Basal cell carcinoma (SCC)
Malignant melanoma (MM)
Squamous cell carcinoma (SCC)
- UV exposure
- Chronic inflammation eg wound scars, immunosuppression
Basal cell carcinoma (BCC)
- UV exposure
- Skin type 1 (burns doesn’t tan)
- Ageing
Malignant melanoma (MM) - UV exposure - Alcohol drinking - Affluence - Red hair - High density freckles - Skin type 1 (burns doesn't tan) - -Atypical moles - Sun sensitivity Pale skin - Family history - Immunosuppression
squamous cell carcinoma (scc)
- presents when
- presents how
- tumour of?
- features inc how aggressive
- commonness
- Present later in life
- Locally invasive, malignant tumour of squamous keratinocytes (outermost bit of epidermis)
- More aggressive than BCC as has higher metastatic potential - particularly to lymph nodes (but still rare to metastasise)
- 2nd most common (to BCC)
- On sun exposed sites
- Ill defined nodules
- May ulcerate
- Grow rapidly
basal cell carcinoma (bcc)
- presents when
- presents where
- presents how
- tumour of?
- features inc how aggressive
- commonness
- Tumour of basal keratinocytes (deepest bit of epidermis)
- Most common malignant skin cancer
- Non pigmented mostly. If pigmented, can resemble melanoma
- Majority in elderly
- Majority head and neck
- May ulcerate (=rodent lesion)
- Border of ulcerated lesion is raised with pearly appearance
- Shiny nodule
- Non pigmented mainly
- Bleeds following minor trauma and does not heal
- less aggressive and metastatic than SCC– slow growing, slowly causing local tissue destruction
malignant melanoma (mm)
- tumour of?
- presents when
- presents where
- presents how
- prognosis inc bad prognosis signs
- features inc how aggressive
- commonness
- types (4)
- Most malignant
— Tumour of melanocytes
in basal layer of epidermis
—Produce melanin
—Absorbs UV (protective) - rarest out of MM, SCC, BCC
- younger patients
- Often fatal
- Bad prognosis signs
— Thick lesions
— Over 60 y
— Male
— Ulceration of lesion
— On trunk - Men - back/chest
Women - lower legs - Most lesions have dark colour, almost black in parts
Types
- Superficial spreading (SSMM- large, flat (laterally growth not vertical))
- Nodular (most aggressive)
- Lentigo maligna (face, slow growing)
- Acral (palms/soles)
skin cancer investigations
A- asymmetrical shape B- border irregularity C- colour irregularity D- diameter >6mm E- elevation,
Major = Change / evolution is key -- Size, shape, colour (usually darkening) Minor = -- Inflammation -- Crusting -- Bleeding -- Sensory change- inc itching
Feel lymph nodes
skin cancer management
Surgical excision - wide borders (minimal 5mm) and histology
Radiotherapy (esp if non resectable/ not fit for surgery)
Superficial ones (esp BCC)
- –Cryotherapy
- –Photodynamic therapy
Metastatic (esp MM)
- –Remove regional lymph nodes
- –Radiotherapy
- –Immunotherapy
- –Chemotherapy
- –Isolated limb perfusion - limb circulation temporarily disconnected from body. External pump includes chemo that circulates to only particular limb
