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Phase 3 > Week 10 > Flashcards

Week 10 Flashcards

1
Q

What is the term for hypo pigmented patches of skin?

A

vitiligo

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2
Q

What are the 3 main functions of the skin?

A

protection
regulation
sensation

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3
Q

Describe the barrier function of the skin

A 
physical and immunological
mechanical impacts 
protects and detects pressure
barrier to micro-organisms 
barrier to radiation and chemicals
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4
Q

Describe the physiological regulation of the skin

A

body temperature via sweat and hair
changes in peripheral circulation
fluid balance via sweat
synthesis of vitamin D

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5
Q

What are the layers of the epidermis?

A

stratum corner
stratum granulosum
stratum spinous
stratum basale

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6
Q

What germ layer does skin originate from?

A

ectoderm

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7
Q

Describe the embryology of the skin

A

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

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8
Q

Describe the immune system of the skin

A

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

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9
Q

Describe the effects of UV on the skin

A

direct cellular damage and alterations in immunological function
photoaging
DNA damage
carcinogenesis

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10
Q

What does chronic UV exposure lead to?

A

loss of skin elasticity
fragility
abnormal pigmentation and haemorrhage of blood vessels
wrinkles and premature ageing

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11
Q

Describe vitamin D absorption in the skin

A

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)

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12
Q

What conditions are associated with vitamin D deficiency?

A

common cancers
autoimmune diseases
infective disease
cardiovascular disease

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13
Q

Describe Merkel cells

A

at the base of the epidermis, respond to sustained gentle and localised pressure

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14
Q

Describe meissner corpsucles

A

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

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15
Q

Describe ruffini’s corpuscles

A

situated in the dermis

receptors sensitive to deep pressure and stretchin

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16
Q

Describe pacinian corpuscles

A

mechanoreceptors present deep in the dermis

sensitive only to deep touch, rapid deformation of skin surface and around joints for proprioception

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17
Q

What do free nerve endings sense?

A

pain

temperature

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18
Q

What is a macule?

A

flat patch

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19
Q

What is a papule?

A

raised lump (0.5cm-1cm)

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20
Q

What is a pustule?

A

small, raised, pus filled

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21
Q

What is a plaque?

A

raised macule

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22
Q

What is a vesicle?

A

tiny bubble
no pus - clear serous fluid
chicken pox

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23
Q

What is a bulla?

A

large vesicle

large blister

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24
Q

What is ulceration?

A

loss of epidermis over area of skin

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25
Q

Describe the aetiology of acne

A

keratin and thick sebum blockage of sebaceous gland
androgenic increases sebum production and viscosity
proprioni bacterium inflammation

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26
Q

What are the clinical features of acne?

A 
papules
pustules
erythema
comedones
nodules
cysts
scarring
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27
Q

What are the subtypes of acne?

A 
papulopustular
nodulocystic
comedonal
steroid induced
acne fulminans
acne agminata
acne rosacea
acne inversus
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28
Q

What is the most common type of acne?

A

papulopustular

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29
Q

What are the mechanisms that can be used to treat acne?

A

reduce plugging
reduce bacteria
reduce sebum production

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30
Q

how is plugging reduced?

A

topical retinoid

topical benzoyl peroxide

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31
Q

How is bacteria reduced in acne?

A 
topical antibiotics (erythromycin, clindamycin)
oral antibiotics (tetracyclines, erythromycin)
benzoyl peroxide reduced bacterial resistance
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32
Q

how is sebum production reduced?

A

hormones - anti androgen - dianette ? OCP

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33
Q

What are the side effects of acne treatment?

A

irritant, burning, peeling, bleaching
oral antibiotics - GI upset
OCP - possible DVT risk

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34
Q

Describe oral isotretinoin

A 
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
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35
Q

Describe eczema

A

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

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36
Q

What are the endogenous types of dermatitis?

A 
atopic
seborrhoea
discoid
varicose
pompholyx
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37
Q

What are the exogenous types of eczema?

A

contact (allergic, irritant)

photoreactions (allergic, drug)

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38
Q

Describe atopic eczema

A

itchy inflammatory skin condition
associated with asthma, allergic rhinitis, conjunctivitis, hayfever
high IgE immunoglobulin antibody levels
genetic and immune aetiology

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39
Q

Describe infant atopic eczema

A 
itchy
occasionally vesicluar 
often facial component 
secondary infection
<50% still have eczema by 18 months
occasionally aggravated by food (milk)
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40
Q

What are the complications of atopic eczema?

A

bacterial infection - staph.aureas
viral infection - molluscum, viral warts, eczema herpeticum
growth reduction
psychological impact

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41
Q

What is the management of atopic eczema?

A 
emollients
topical steroids
bandages
antihistamines
antibiotics/antivirals
education
avoidance of exacerbating factors
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42
Q

describe contact dermatitis

A

precipitated by an exogenous agent
irritant - direct noxious effect on skin battier
allergic - type IV hypersensitivity reaction

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43
Q

What are common allergens that can cause contact dermatitis?

A

nickel -jewellwery, zips, scissors, coins
chromate - cement, tanned leather
cobalt - pigment
colophony - glue, adhesive tape, plasters
fragrance - cosmetics, creams, soaps

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44
Q

Describe seborrhoea dermatitis

A 
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
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45
Q

What is the management of seborrhoeic dermatitis?

A

scalp - medicated anti yeast shampoo

face - anti-microbial, mild steroid, simple moisturiser

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46
Q

describe venous dermatitis

A

underlying venous disease
affects lower legs
incompetence of deep perforating veins
increased hydrostatic pressure

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47
Q

Describe the management of venous dematitis

A

emollient
mild/moderate topical steroid
compression bandage / stockings
consider venous surgical intervention

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48
Q

What is psoriasis?

A

a chronic relapsing and remitting scaling skin disease which may appear at any age and affect any part of the skin

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49
Q

What causes psoriasis?

A

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

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50
Q

What is psoriasis linked to?

A

psoriatic arthritis
metabolic syndrome
liver disease / alcohol misuse
depression

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51
Q

what genes are associated with psoriasis?

A

PSORS1

HLA - Cw0602

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52
Q

What types of psoriasis are there?

A 
plaque
guttate
pustular 
erythrodermic 
palmar / plantar pustulosis
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53
Q

What happens in a psoriatic nail?

A

nail lifts off distal edge

nail pitting

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54
Q

Describe guttate psoriasis

A

small patches

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55
Q

What are the treatment options for psoriasis?

A 
topical creams and ointments
phototherapy light treatment
acitrecin 
methotrexate 
ciclosporin
biological therapies _ infliximab, etarnercept, adalimimab
56
Q

Describe ultraviolet phototehrapy

A 
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
57
Q

Describe the systemic therapy options in psoraisis

A 
immunosuppressants - methotrexate, ciclosporin 
oral retinoids
hydroxycarbamide
fumaric acid esters
biologics - infliximab (TNF)
58
Q

Give an overview of the 2 main pathways that interact or converge to cause skin cancer

A

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

59
Q

What are the main types of skin cancer?

A

basal cell
squamous cell
malignant melanoma

60
Q

Describe basal cell carcinoma

A

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

61
Q

What are the subtypes of BCC?

A

nodular
superficial
pigmented
morphoeic / sclerotic

62
Q

describe the appearance of a nodular BCC

A

nodule >0.5cm raised lesion
shiny “pearly”
telangiectasia
often ulcerated centrally

63
Q

Describe the treatment of basal cell carcinoma

A 
gold standard - surgical excision - 3-4mm margin
curettage and cautery
cryotherapy
photodynamic therapy
topical imiquimod / 5-flurouracil cream
mohs micrographic surgery
64
Q

Describe squamous cell carcinoma

A

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

65
Q

What is the treatment of squamous cell carcinoma?

A 
surgical excision 4mm margin
curettage and cautery 
pre-malignat / squamous cell in situ
topical imiquimod  / 5-fluorouracil cream
cryotherapy
photodynamic therapy 
sun protection
66
Q

Describe melanoma

A 
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
67
Q

What are some risk factors for melanoma?

A 
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
68
Q

What are the subtypes of melanoma?

A 
superficial spreading malignant melanoma 
nodular melanoma 
acral melanoma
subungual melanoma
amelanotic melanoma
lentigo maligna - precursor 
lentigo maligna melanoma
melanoma in situ
69
Q

What is the treatment of melanoma?

A

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

70
Q

Give examples of cutaneous tumour syndromes

A

gorlin’s
brook spiegler
gardner
Cowden’s

71
Q

Describe gorlin’s syndrome

A

multiple BCCs
jaw cysts
risk of breast cancer

72
Q

describe brook spieler syndrome

A

multiple BCCs

trichoepitheliomas

73
Q

Describe gardner syndrome

A

soft tissue tumours, polyps, bowel cancers

74
Q

Describe cowden’s syndrome

A

multiple hamartomas
thyroid
breast cancers

75
Q

Describe the microbiome of the skin

A

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

76
Q

Describe impetigo

A

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

77
Q

Describe tinea

A

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

78
Q

Describe soft tissue abscesses

A

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

79
Q

Describe cellultis

A

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

80
Q

How is cellulitis classified?

A

enron classification

81
Q

Describe enron classification

A

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

82
Q

How should enron class Ia patients be treated?

A

oral therapy usually
1st line - flucloxacillin 1g 6 hourly
2nd line - doxycycline 100mg bd
usual treatment duration 7 days

83
Q

How should enron class Ib and II be treated?

A

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

84
Q

Describe ambulatory care in cellulitis treatment

A

once daily antibiotics given in care unit or at patient’s home
usually IV ceftriaxone 2g od

85
Q

How should patients with class III and IV enron cellulitis be treated?

A

hospital admission for IV therapy and consideration of surgical management
complications can be severe tissue destruction or septic shock

86
Q

Describe streptococcal toxic shock

A

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

87
Q

Describe the treatment of step toxic shock

A

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

88
Q

Describe necrotising fasciitis

A

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

89
Q

Describe the signs / symptoms of necrotising fasciitis

A 
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)
90
Q

Describe type 1 necrotising fasciitis

A

polymicrobial
usually complicates existing wounds, including surgical wounds
microbiology usually a mix of positive, negative and anaerobes

91
Q

Describe type 2 necrotising fasciitis

A

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

92
Q

Describe the treatment of necrotising fasciitis

A

requires broad spectrum antibiotic therapy - flucloxacillin, benzylpenicillin, gentamicin, clindamicin, metronidazole
surgical intervention is the most important

93
Q

Describe bite injuries

A

penetrating injuries involving vulnerable structures (hands)
altered microbiology of wounds (staph and strep still common, anaerobes common, pastuerella and capnoctophagia from mammal bites)

94
Q

What is the treatment of bite wounds?

A

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

95
Q

Describe soft tissue infections in people who inject drugs

A

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

96
Q

Describe PVL staph

A

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

97
Q

Describe the treatment of PVL staph

A

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

98
Q

Describe herpes simplex virus

A

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

99
Q

Describe chicken pox

A

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

100
Q

Describe shingles

A

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

101
Q

What can changes in the skin be a marker of?

A 
endocrine disease
internal malignancy 
nutritional deficiency
systemic infection
systemic inflammatory disease
102
Q

What endocrine conditions can lead to skin changes?

A

thyroid
diabetes
cushings / steroid excess
sex hormones

103
Q

What skin changes can be seen in hypothyroidism?

A

dry skin

104
Q

What skin changes can be seen in hyperthyroidism?

A 
thyroid dermopathy (pre-tibial myxoedema)
thyroid acropachy
105
Q

What skin changes can be seen in diabetes?

A 
necrobiosis lipoidica
diabetic dermopathy
sclerodema
leg ulcers
granuloma annulare
106
Q

Describe necrobiosis lipoidica

A

waxy appearance
usually yellow discolouration
often shins
occassionally ulcerates and scars

107
Q

Describe sclerodema

A 
feels a bit like orange peel
surface can be dimpled 
inflammatory - warm
blanching
shoulder - shawl distribution
108
Q

Describe diabetic ulcers

A 
foot ulcers - 
neuropathic 
over pressure points on feet
venous ulcers- 
multifactorial 
peripheral vascular disease 
venous eczema
109
Q

Describe granuloma annulare

A

round
backs of hands and feet
if widespread check for diabetes

110
Q

What skin changes can be as a result of cushings / steroid excess?

A

acne
striae
erythema
gynaecomastia

111
Q

What skin changes can be seen in addisons?

A

hyper pigmentation

acanthosis nigracans

112
Q

Describe the general changes that occur in cushing’s disease

A

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

113
Q

What skin changes can excess testosterone lead to and how is this caused?

A 
acne
hirsutism
PCOS
testicular tumours
testosterone drug therapy
114
Q

What skin changes can excess progesterone lead to and how is this caused?

A

acne
dermatitis
congenital adrenal hyperplasia
contraceptive treatment

115
Q

What skin changes can be seen in internal malignancy?

A 
necrolytic migratory erythema
erythema gyratum reopens
acanthosis nigricans
erythema annulare
sweet's syndrome
sister mary jospeph nodule
116
Q

Describe necrolytic migratory erythema

A

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

117
Q

Describe erythema gyratum repens

A

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

118
Q

Describe acanthosis nigricans

A

smooth, velvet like, hyperkeratotic plaques in intertriginous areas
type 1 - malignancy
type 2 - familial
type 3 - obesity and insulin resistance

119
Q

Describe vitamin B 6 deficiencies

A

pyridoxine

dermatitis

120
Q

Describe vitamin B 12 deficiencies

A

cobalamin

angular chelitis

121
Q

Describe vitamin B 3 deficiencies

A

niacin

pellagra (dementia, dermatitis, diarrhoea)

122
Q

Describe zinc deficiency

A 
acrodermatitis enteropathica
inherited or acquired condition
pustules, bull, scarring 
inherited 
alcoholism
malabsorption states
IBD
bowel surgery
123
Q

Describe vitamin C deficiency

A 
punctate purpura / brusing
corkscrew spiral curly hairs
patchy hyperpigmentation 
dry skin
dry hair
non healing wounds
inflamed gums
124
Q

Describe erythema nodosum

A 
streptococcal infection
pregnancy / oral contraceptive
sacrcoidosis
drug induced
bacterial / viral infection
others
125
Q

Describe pyoderma gangrenosum

A

ulcer with purple overhanging

associated with IBD, RA, myeloma

126
Q

What types of drug reactions are there?

A 
maculopapular
urticaria
morbilliform
papulosquamous
photo-toxic
pustular
lichenoid
fixed drug rash
bullous
itch
127
Q

What drugs commonly cause acute rashes?

A 
antibiotics
NSAIDs
chemotherapeutic agents
psychotropic 
anti-epileptic - lamitrigine, carbamazepine
cardiac
128
Q

Describe vasculitis

A

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

129
Q

Give examples of blistering disorders

A 
drug induced - steven johnson syndrome
toxic epidermal necrolysis
immunobullous diseases
bullous pemphigoid
bullous pemphigus
130
Q

Describe toxic epidermal necrolysis (TEN)

A 
dermatological emergency
majority drug induced
most severe mucous membrane involvement
stop suspect drug
fluid balance
SCORTEN severity scale
131
Q

describe eryhtema multiforme

A 
self limiting allergic reaction
HSV, EBV, occasionally drug
no or mild prodromme
target lesions
never progresses to TEN
132
Q

What is the difference between bullous pemphigoid and pemphigus vulgaris

A

pemphigoid is deep

pemphigus is superficial

133
Q

What is the treatment of immunobullous disorders?

A

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

134
Q

What is the treatment of dermatitis herpetiformis?

A

topical steroids
gluten free diet
oral dapsone

135
Q

Describe urticaria

A 
itchy, wheals
lesions last <24 hours
non-scarring
common
acute <6 weeks
chronic >6 weeks
immune mediated 
type 1 allergic IgE response
136
Q

What is the treatment of urticaria?

A

antihistamines
steroids
immunosuppresion
omilizumab

137
Q

Describe erythroderma

A 
descriptive term
>80% involvement 
erythema 
psoriasis
eczema
cutaneous lymphoma
drug reaction
treat underlying skin disorders

Phase 3 (15 decks)

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