Week 10 Flashcards
What is the term for hypo pigmented patches of skin?
vitiligo
What are the 3 main functions of the skin?
protection
regulation
sensation
Describe the barrier function of the skin
physical and immunological mechanical impacts protects and detects pressure barrier to micro-organisms barrier to radiation and chemicals
Describe the physiological regulation of the skin
body temperature via sweat and hair
changes in peripheral circulation
fluid balance via sweat
synthesis of vitamin D
What are the layers of the epidermis?
stratum corner
stratum granulosum
stratum spinous
stratum basale
What germ layer does skin originate from?
ectoderm
Describe the embryology of the skin
5th week - the skin of the embryo is covered by simple cuboidal epithelium
7th week - single squamous layer (periderm) and a basal layer
4th month - intermediate later containing several layers, is interposed between the periderm and the basal cells
early foetal period the epidermis is invaded by melanoblasts, cells of neural crest origin
hair - 3rd month as an epidermal proliferation into the dermis
cells of the epithelial root sheath proliferate to form a sebaceous gland bud
sweat glands develop as down growths of epithelial cords into dermis
Describe the immune system of the skin
langerhans ells are dendritic cells, residing in the basal layers
present to naive T cells in lymph nodes to initiate the adaptive immune response
cytokine release cascade
Describe the effects of UV on the skin
direct cellular damage and alterations in immunological function
photoaging
DNA damage
carcinogenesis
What does chronic UV exposure lead to?
loss of skin elasticity
fragility
abnormal pigmentation and haemorrhage of blood vessels
wrinkles and premature ageing
Describe vitamin D absorption in the skin
UVB photons are absorbed by 7-dehydrocholesterol in the skin and converted to previtamin D(3)
Pre vitamin D(3) undergoes transformation within the plasma membrane to active vitamin D(3)
What conditions are associated with vitamin D deficiency?
common cancers
autoimmune diseases
infective disease
cardiovascular disease
Describe Merkel cells
at the base of the epidermis, respond to sustained gentle and localised pressure
Describe meissner corpsucles
situated immediately below the epidermis and are particularity well represented on the palmar surfaces of the fingertips and the lips
especially sensitive to light touch
Describe ruffini’s corpuscles
situated in the dermis
receptors sensitive to deep pressure and stretchin
Describe pacinian corpuscles
mechanoreceptors present deep in the dermis
sensitive only to deep touch, rapid deformation of skin surface and around joints for proprioception
What do free nerve endings sense?
pain
temperature
What is a macule?
flat patch
What is a papule?
raised lump (0.5cm-1cm)
What is a pustule?
small, raised, pus filled
What is a plaque?
raised macule
What is a vesicle?
tiny bubble
no pus - clear serous fluid
chicken pox
What is a bulla?
large vesicle
large blister
What is ulceration?
loss of epidermis over area of skin
Describe the aetiology of acne
keratin and thick sebum blockage of sebaceous gland
androgenic increases sebum production and viscosity
proprioni bacterium inflammation
What are the clinical features of acne?
papules pustules erythema comedones nodules cysts scarring
What are the subtypes of acne?
papulopustular nodulocystic comedonal steroid induced acne fulminans acne agminata acne rosacea acne inversus
What is the most common type of acne?
papulopustular
What are the mechanisms that can be used to treat acne?
reduce plugging
reduce bacteria
reduce sebum production
how is plugging reduced?
topical retinoid
topical benzoyl peroxide
How is bacteria reduced in acne?
topical antibiotics (erythromycin, clindamycin) oral antibiotics (tetracyclines, erythromycin) benzoyl peroxide reduced bacterial resistance
how is sebum production reduced?
hormones - anti androgen - dianette ? OCP
What are the side effects of acne treatment?
irritant, burning, peeling, bleaching
oral antibiotics - GI upset
OCP - possible DVT risk
Describe oral isotretinoin
oral retinoid for severe acne concentrated vitamin A reduces sebum, plugging and bacteria remission in 8-% of teenagers standard course 16 weeks, 1mg/kg dry lips, nose bleed, dry skin, myalgia, deranged LFTs, raised lipids, mood disturbance, teratogenicity pregnancy prevention programme
Describe eczema
inflammation of the skin
combination of genetic, immune and reactivity to a variety of stimuli
abnormalities in skin barrier - increased permeability and reduces its antimicrobial function
filaggrin inherited abnormality is linked
What are the endogenous types of dermatitis?
atopic seborrhoea discoid varicose pompholyx
What are the exogenous types of eczema?
contact (allergic, irritant)
photoreactions (allergic, drug)
Describe atopic eczema
itchy inflammatory skin condition
associated with asthma, allergic rhinitis, conjunctivitis, hayfever
high IgE immunoglobulin antibody levels
genetic and immune aetiology
Describe infant atopic eczema
itchy occasionally vesicluar often facial component secondary infection <50% still have eczema by 18 months occasionally aggravated by food (milk)
What are the complications of atopic eczema?
bacterial infection - staph.aureas
viral infection - molluscum, viral warts, eczema herpeticum
growth reduction
psychological impact
What is the management of atopic eczema?
emollients topical steroids bandages antihistamines antibiotics/antivirals education avoidance of exacerbating factors
describe contact dermatitis
precipitated by an exogenous agent
irritant - direct noxious effect on skin battier
allergic - type IV hypersensitivity reaction
What are common allergens that can cause contact dermatitis?
nickel -jewellwery, zips, scissors, coins
chromate - cement, tanned leather
cobalt - pigment
colophony - glue, adhesive tape, plasters
fragrance - cosmetics, creams, soaps
Describe seborrhoea dermatitis
chronic, scaly inflammatory condition often thought to be dandruff face, scalp, eyebrows overgrowth of pityrosporum oval yeast can be worse in teenagers occasionally confused with psoriasis
What is the management of seborrhoeic dermatitis?
scalp - medicated anti yeast shampoo
face - anti-microbial, mild steroid, simple moisturiser
describe venous dermatitis
underlying venous disease
affects lower legs
incompetence of deep perforating veins
increased hydrostatic pressure
Describe the management of venous dematitis
emollient
mild/moderate topical steroid
compression bandage / stockings
consider venous surgical intervention
What is psoriasis?
a chronic relapsing and remitting scaling skin disease which may appear at any age and affect any part of the skin
What causes psoriasis?
T cell mediated autoimmune disease
abnormal infiltration of T cells - release of inflammatory cytokines including interferon, interleukins and TNF
increased keratinocyte proliferation
environmental and genetic factors
What is psoriasis linked to?
psoriatic arthritis
metabolic syndrome
liver disease / alcohol misuse
depression
what genes are associated with psoriasis?
PSORS1
HLA - Cw0602
What types of psoriasis are there?
plaque guttate pustular erythrodermic palmar / plantar pustulosis
What happens in a psoriatic nail?
nail lifts off distal edge
nail pitting
Describe guttate psoriasis
small patches
What are the treatment options for psoriasis?
topical creams and ointments phototherapy light treatment acitrecin methotrexate ciclosporin biological therapies _ infliximab, etarnercept, adalimimab
Describe ultraviolet phototehrapy
non specific immunosuppressant therapy can reduce t cell proliferations encourages vitamin D (reduces skin turnover) UV-B light most commonly used risks - burning, skin cancer
Describe the systemic therapy options in psoraisis
immunosuppressants - methotrexate, ciclosporin oral retinoids hydroxycarbamide fumaric acid esters biologics - infliximab (TNF)
Give an overview of the 2 main pathways that interact or converge to cause skin cancer
1) direct action of UV on target cells (keratinocytes) for neoplastic transformation via DNA damage
2) effects of UV on the host’s immune system
What are the main types of skin cancer?
basal cell
squamous cell
malignant melanoma
Describe basal cell carcinoma
most common type of skin cancer
basal cells multiply rapidly due to mutated DNA and continue growing when would normally die, accumulating abnormal cells form a tumour
PTCH gene mutation may predispose
mainly in head/neck - sun exposed sites
rarely metastasis or kills
3/10 caucasians will develop BCC within their lifetime
What are the subtypes of BCC?
nodular
superficial
pigmented
morphoeic / sclerotic
describe the appearance of a nodular BCC
nodule >0.5cm raised lesion
shiny “pearly”
telangiectasia
often ulcerated centrally
Describe the treatment of basal cell carcinoma
gold standard - surgical excision - 3-4mm margin curettage and cautery cryotherapy photodynamic therapy topical imiquimod / 5-flurouracil cream mohs micrographic surgery
Describe squamous cell carcinoma
may occur in normal skin or skin that has been injured or chronically inflamed
originates from keratinocytes
2nd commonest skin cancer
pre malignant variants - actinic keratoses, Bowens disease
mostly in sun exposed areas of skin
metastasis risk from high risk SCC is 10-30%
high risk sites - ears, lips
What is the treatment of squamous cell carcinoma?
surgical excision 4mm margin curettage and cautery pre-malignat / squamous cell in situ topical imiquimod / 5-fluorouracil cream cryotherapy photodynamic therapy sun protection
Describe melanoma
malignant tumour of melanocytes most common in skin accounts for 75% skin cancer deaths DNA damage - mainly UV, rarely genetic radial growth phase, then vertical growth depth of presentation determines the prognosis spread via lymphatics premalignant form
What are some risk factors for melanoma?
genetic markers (CDKN2A) family history of dysplastic nevi or melanoma ultraviolet irradiation sunburns during childhood sun exposure and fair skin congenital nevi multiple nevi equatorial latitudes DNA repair defects immunosuppression
What are the subtypes of melanoma?
superficial spreading malignant melanoma nodular melanoma acral melanoma subungual melanoma amelanotic melanoma lentigo maligna - precursor lentigo maligna melanoma melanoma in situ
What is the treatment of melanoma?
surgical excision (breslow <1mm - 1cm margin,
breslow > 1mm - 2 cm margin)
if metastatic -chemotherapy, isolated limb perfusion
vaccine therapy
biologic antibodies to vascular growth factors (bevacizumab) or BRAF genetic defects (vemurafenib)
long term follow up
assessment for lymph node / organ spread
genetic testing
Give examples of cutaneous tumour syndromes
gorlin’s
brook spiegler
gardner
Cowden’s
Describe gorlin’s syndrome
multiple BCCs
jaw cysts
risk of breast cancer
describe brook spieler syndrome
multiple BCCs
trichoepitheliomas
Describe gardner syndrome
soft tissue tumours, polyps, bowel cancers
Describe cowden’s syndrome
multiple hamartomas
thyroid
breast cancers
Describe the microbiome of the skin
coagulase negative staph
corynebacterium sp.
less acidic areas - staph. aureas, strep pyrogenes
usually not gram negative bacteria or anaerobic organisms
anaerobe P.acnes occurs in sweat and sebaceous glands
normal skin also colonised with fungi and mites
Describe impetigo
golden encrusted skin lesions with inflammation localised to the dermis
most common in children
contagious and may occur in small outbreaks
caused by staph.aureas an usually mild and self limiting
can treat with topical fusidic acid or systemic antibiotics if required
Describe tinea
superficial fungal infection of the skin or nails
very common, particularly on the feet
most common causes 0 microsporum, epodermophyton, trichophyton
treatment with topical therapy in non severe cases - terbinafine cream
systemic therapy in severe cases and those involving hair / nails
- terbainfine pr itraconazole
Describe soft tissue abscesses
infection within the dermis or fat layers with development of walled off infection and pooled pus
limited antibiotic penetration into abscess
best treatment is always surgical drainage
antibiotics not usually required if abscess fully drained and no surrounding cellulitis
Describe cellultis
infection involving dermis
most commonly begins on the lower limbs
often tracks through the lymphatic system and may involve localised lymph nodes
may be associated with systemic upset although bacteraemia is relatively uncommon
usually caused by beta-haemolytic streptococci (group A strep) and Staph aureas
How is cellulitis classified?
enron classification
Describe enron classification
I. patient not systemically unwell and no significant co-morbidities
II. patient systemically unwell or has significant co-morbiditeis which may complicate or delay resolution of infection
III. patient has signifiant systemic upset of unstable co-morbidities that will interfere with response to treatment or limb threatening vascular compromise
IV. presence of sepsis or severe, life threatening complications
How should enron class Ia patients be treated?
oral therapy usually
1st line - flucloxacillin 1g 6 hourly
2nd line - doxycycline 100mg bd
usual treatment duration 7 days
How should enron class Ib and II be treated?
initial IV therapy usually appropriate
1st line - flucloxacillin 2g 6 hourly
2nd line - vancomycin based on dosing calculations
usually switched to oral therapy after 48-72 hours
Describe ambulatory care in cellulitis treatment
once daily antibiotics given in care unit or at patient’s home
usually IV ceftriaxone 2g od
How should patients with class III and IV enron cellulitis be treated?
hospital admission for IV therapy and consideration of surgical management
complications can be severe tissue destruction or septic shock
Describe streptococcal toxic shock
caused by toxin producing group A strep
primary infection typically within the throat or skin / soft tissue
patients present with localised infection (not necessarily severe) fever and shock
often have diffuse, fain rash over body / limbs
Describe the treatment of step toxic shock
surgery - aggressively seek out abscess for drainage
antibiotics - penicillin may be ineffective, add clindamycin to reduce toxin production
consider pooled human immunoglobulin in severe cases
Describe necrotising fasciitis
immediately life threatening soft tissue infection with deep tissue involvement
rapidly progressive with extensive tissue damage requiring extensive surgical debridement
surgical emergency - do not delay consulting a surgeon
Describe the signs / symptoms of necrotising fasciitis
rapidly progressive pain out of proportion to clinical signs severe systemic upset presence of visible necrotic tissue imaging may demonstrate fascial oedema and gas in soft tissues (this is a late sign, cannot exclude nec fasc)
Describe type 1 necrotising fasciitis
polymicrobial
usually complicates existing wounds, including surgical wounds
microbiology usually a mix of positive, negative and anaerobes
Describe type 2 necrotising fasciitis
group a streptococcus
usually occurs in previous healthy tissue, typically on the limbs
may follow a minor injury such as a scratch or sprain
microbiology usually monobacterial infection with streptococcus pyrogenes only
Describe the treatment of necrotising fasciitis
requires broad spectrum antibiotic therapy - flucloxacillin, benzylpenicillin, gentamicin, clindamicin, metronidazole
surgical intervention is the most important
Describe bite injuries
penetrating injuries involving vulnerable structures (hands)
altered microbiology of wounds (staph and strep still common, anaerobes common, pastuerella and capnoctophagia from mammal bites)
What is the treatment of bite wounds?
antibiotics treatment co-amoxiclav or doxycycline and metronidazole
surgical treatment
prophylactic treatment - antibiotics for high risk injuries, consideration of tetanus prophylaxis
rabies is bat scratches or bites only in the Uk
Describe soft tissue infections in people who inject drugs
often present late with neglected soft tissue infection
staph.aureas predominates but infections are often polymicrobial
high rates of bacteraemia and disseminated infection - triad of staph aureas, DVT and multiple pulmonary abscesses
must offer BBV testing on every admission
Describe PVL staph
virulence factor carried by some staph aureas
association with recurrent soft tissue boils and abscesses often over months or yearss
transmissible - outbreaks in people living together
rarely associated with severe necrotising pneumonia
obtain cultures and ask lab to do PVL genotyping
Describe the treatment of PVL staph
surgical treatment of abscesses
antibiotics - outside of UK often MRSA, Uk usually MSSA,
clindamycin to reduce toxin production
decolonisation therapy for patient and contacts - topical chlohexidane for skin / hair. nasal mupirocin ointment, simultaneous washing of sheets / towels
Describe herpes simplex virus
primary infection asymptomatic in 60%
type 1 - stomatitis
type 2 -genital herpes
recurrent - virus latent in sensory nerve ganglia
diagnosis - clinical
treatment - acyclovir - topical, oral, IV
Describe chicken pox
Varicella zoster virus
often self limiting childhood infection
highly infectious
contagious from days 8-21 (symptoms from day 10)
diagnosed by PCR
of vesicle fluid
congenital abnormalities if acquired during pregnancy
problematic in adults -pneumonitis
at risk adults are treated with acyclovir
Describe shingles
reactivation of dormant VZV (dorsal root ganglia)
dermatomal Distribution
transmissible - isolate until last crop of vesicles crusted
may be very painful
treat high risk patients with acyclovir
pain management - NSAIDs, garbapentin
What can changes in the skin be a marker of?
endocrine disease internal malignancy nutritional deficiency systemic infection systemic inflammatory disease
What endocrine conditions can lead to skin changes?
thyroid
diabetes
cushings / steroid excess
sex hormones
What skin changes can be seen in hypothyroidism?
dry skin
What skin changes can be seen in hyperthyroidism?
thyroid dermopathy (pre-tibial myxoedema) thyroid acropachy
What skin changes can be seen in diabetes?
necrobiosis lipoidica diabetic dermopathy sclerodema leg ulcers granuloma annulare
Describe necrobiosis lipoidica
waxy appearance
usually yellow discolouration
often shins
occassionally ulcerates and scars
Describe sclerodema
feels a bit like orange peel surface can be dimpled inflammatory - warm blanching shoulder - shawl distribution
Describe diabetic ulcers
foot ulcers - neuropathic over pressure points on feet venous ulcers- multifactorial peripheral vascular disease venous eczema
Describe granuloma annulare
round
backs of hands and feet
if widespread check for diabetes
What skin changes can be as a result of cushings / steroid excess?
acne
striae
erythema
gynaecomastia
What skin changes can be seen in addisons?
hyper pigmentation
acanthosis nigracans
Describe the general changes that occur in cushing’s disease
increased central adiposity
moon faces and buffalo hump
global skin atrophy, epidermal and dermal components
striae on abdominal flanks, arms, thighs
purpura with minor trauma - reduced connective tissue
What skin changes can excess testosterone lead to and how is this caused?
acne hirsutism PCOS testicular tumours testosterone drug therapy
What skin changes can excess progesterone lead to and how is this caused?
acne
dermatitis
congenital adrenal hyperplasia
contraceptive treatment
What skin changes can be seen in internal malignancy?
necrolytic migratory erythema erythema gyratum reopens acanthosis nigricans erythema annulare sweet's syndrome sister mary jospeph nodule
Describe necrolytic migratory erythema
glucagonoma syndrome
rare disease
erythematous, scaly plaques on aural, interiginous and periorificial areas
islet cell tumours of the pancreas
also hyperglycaemia, diarrhoea, weight loss, glossitis
treatment is removal of the tumour
Describe erythema gyratum repens
rare
very distinctive
reddened concentric bands whorled woodgrain pattern
severe pruritus and peripheral eosinophilia
strong association with lung cancer
also with breast, cervical, GI cancers less strong
Describe acanthosis nigricans
smooth, velvet like, hyperkeratotic plaques in intertriginous areas
type 1 - malignancy
type 2 - familial
type 3 - obesity and insulin resistance
Describe vitamin B 6 deficiencies
pyridoxine
dermatitis
Describe vitamin B 12 deficiencies
cobalamin
angular chelitis
Describe vitamin B 3 deficiencies
niacin
pellagra (dementia, dermatitis, diarrhoea)
Describe zinc deficiency
acrodermatitis enteropathica inherited or acquired condition pustules, bull, scarring inherited alcoholism malabsorption states IBD bowel surgery
Describe vitamin C deficiency
punctate purpura / brusing corkscrew spiral curly hairs patchy hyperpigmentation dry skin dry hair non healing wounds inflamed gums
Describe erythema nodosum
streptococcal infection pregnancy / oral contraceptive sacrcoidosis drug induced bacterial / viral infection others
Describe pyoderma gangrenosum
ulcer with purple overhanging
associated with IBD, RA, myeloma
What types of drug reactions are there?
maculopapular urticaria morbilliform papulosquamous photo-toxic pustular lichenoid fixed drug rash bullous itch
What drugs commonly cause acute rashes?
antibiotics NSAIDs chemotherapeutic agents psychotropic anti-epileptic - lamitrigine, carbamazepine cardiac
Describe vasculitis
triggers- infection, drugs, connective tissue disease in RA
check for systemic vasculitis ie renal BP / urinalysis
often localised and not rapidly progressive
less unwell than in meningococcal rash
Give examples of blistering disorders
drug induced - steven johnson syndrome toxic epidermal necrolysis immunobullous diseases bullous pemphigoid bullous pemphigus
Describe toxic epidermal necrolysis (TEN)
dermatological emergency majority drug induced most severe mucous membrane involvement stop suspect drug fluid balance SCORTEN severity scale
describe eryhtema multiforme
self limiting allergic reaction HSV, EBV, occasionally drug no or mild prodromme target lesions never progresses to TEN
What is the difference between bullous pemphigoid and pemphigus vulgaris
pemphigoid is deep
pemphigus is superficial
What is the treatment of immunobullous disorders?
treatment
reduce autoimmune reactions - oral steroids
steroid sparing agents - azathiopine
burst any blisters
dressings and infection control
check for oral involvement
consider screening for underlying malignancy
What is the treatment of dermatitis herpetiformis?
topical steroids
gluten free diet
oral dapsone
Describe urticaria
itchy, wheals lesions last <24 hours non-scarring common acute <6 weeks chronic >6 weeks immune mediated type 1 allergic IgE response
What is the treatment of urticaria?
antihistamines
steroids
immunosuppresion
omilizumab
Describe erythroderma
descriptive term >80% involvement erythema psoriasis eczema cutaneous lymphoma drug reaction treat underlying skin disorders
