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Week 10 Flashcards

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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
Describe the aetiology of acne
keratin and thick sebum blockage of sebaceous gland androgenic increases sebum production and viscosity proprioni bacterium inflammation
26
What are the clinical features of acne?
``` papules pustules erythema comedones nodules cysts scarring ```
27
What are the subtypes of acne?
``` papulopustular nodulocystic comedonal steroid induced acne fulminans acne agminata acne rosacea acne inversus ```
28
What is the most common type of acne?
papulopustular
29
What are the mechanisms that can be used to treat acne?
reduce plugging reduce bacteria reduce sebum production
30
how is plugging reduced?
topical retinoid | topical benzoyl peroxide
31
How is bacteria reduced in acne?
``` topical antibiotics (erythromycin, clindamycin) oral antibiotics (tetracyclines, erythromycin) benzoyl peroxide reduced bacterial resistance ```
32
how is sebum production reduced?
hormones - anti androgen - dianette ? OCP
33
What are the side effects of acne treatment?
irritant, burning, peeling, bleaching oral antibiotics - GI upset OCP - possible DVT risk
34
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 ```
35
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
36
What are the endogenous types of dermatitis?
``` atopic seborrhoea discoid varicose pompholyx ```
37
What are the exogenous types of eczema?
contact (allergic, irritant) | photoreactions (allergic, drug)
38
Describe atopic eczema
itchy inflammatory skin condition associated with asthma, allergic rhinitis, conjunctivitis, hayfever high IgE immunoglobulin antibody levels genetic and immune aetiology
39
Describe infant atopic eczema
``` itchy occasionally vesicluar often facial component secondary infection <50% still have eczema by 18 months occasionally aggravated by food (milk) ```
40
What are the complications of atopic eczema?
bacterial infection - staph.aureas viral infection - molluscum, viral warts, eczema herpeticum growth reduction psychological impact
41
What is the management of atopic eczema?
``` emollients topical steroids bandages antihistamines antibiotics/antivirals education avoidance of exacerbating factors ```
42
describe contact dermatitis
precipitated by an exogenous agent irritant - direct noxious effect on skin battier allergic - type IV hypersensitivity reaction
43
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
44
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 ```
45
What is the management of seborrhoeic dermatitis?
scalp - medicated anti yeast shampoo | face - anti-microbial, mild steroid, simple moisturiser
46
describe venous dermatitis
underlying venous disease affects lower legs incompetence of deep perforating veins increased hydrostatic pressure
47
Describe the management of venous dematitis
emollient mild/moderate topical steroid compression bandage / stockings consider venous surgical intervention
48
What is psoriasis?
a chronic relapsing and remitting scaling skin disease which may appear at any age and affect any part of the skin
49
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
50
What is psoriasis linked to?
psoriatic arthritis metabolic syndrome liver disease / alcohol misuse depression
51
what genes are associated with psoriasis?
PSORS1 | HLA - Cw0602
52
What types of psoriasis are there?
``` plaque guttate pustular erythrodermic palmar / plantar pustulosis ```
53
What happens in a psoriatic nail?
nail lifts off distal edge | nail pitting
54
Describe guttate psoriasis
small patches
55
What are the treatment options for psoriasis?
``` topical creams and ointments phototherapy light treatment acitrecin methotrexate ciclosporin biological therapies _ infliximab, etarnercept, adalimimab ```
56
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 ```
57
Describe the systemic therapy options in psoraisis
``` immunosuppressants - methotrexate, ciclosporin oral retinoids hydroxycarbamide fumaric acid esters biologics - infliximab (TNF) ```
58
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
59
What are the main types of skin cancer?
basal cell squamous cell malignant melanoma
60
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
61
What are the subtypes of BCC?
nodular superficial pigmented morphoeic / sclerotic
62
describe the appearance of a nodular BCC
nodule >0.5cm raised lesion shiny "pearly" telangiectasia often ulcerated centrally
63
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 ```
64
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
65
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 ```
66
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 ```
67
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 ```
68
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 ```
69
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
70
Give examples of cutaneous tumour syndromes
gorlin's brook spiegler gardner Cowden's
71
Describe gorlin's syndrome
multiple BCCs jaw cysts risk of breast cancer
72
describe brook spieler syndrome
multiple BCCs | trichoepitheliomas
73
Describe gardner syndrome
soft tissue tumours, polyps, bowel cancers
74
Describe cowden's syndrome
multiple hamartomas thyroid breast cancers
75
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
76
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
77
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
78
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
79
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
80
How is cellulitis classified?
enron classification
81
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
82
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
83
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
84
Describe ambulatory care in cellulitis treatment
once daily antibiotics given in care unit or at patient's home usually IV ceftriaxone 2g od
85
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
86
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
87
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
88
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
89
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) ```
90
Describe type 1 necrotising fasciitis
polymicrobial usually complicates existing wounds, including surgical wounds microbiology usually a mix of positive, negative and anaerobes
91
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
92
Describe the treatment of necrotising fasciitis
requires broad spectrum antibiotic therapy - flucloxacillin, benzylpenicillin, gentamicin, clindamicin, metronidazole surgical intervention is the most important
93
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)
94
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
95
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
96
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
97
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
98
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
99
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
100
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
101
What can changes in the skin be a marker of?
``` endocrine disease internal malignancy nutritional deficiency systemic infection systemic inflammatory disease ```
102
What endocrine conditions can lead to skin changes?
thyroid diabetes cushings / steroid excess sex hormones
103
What skin changes can be seen in hypothyroidism?
dry skin
104
What skin changes can be seen in hyperthyroidism?
``` thyroid dermopathy (pre-tibial myxoedema) thyroid acropachy ```
105
What skin changes can be seen in diabetes?
``` necrobiosis lipoidica diabetic dermopathy sclerodema leg ulcers granuloma annulare ```
106
Describe necrobiosis lipoidica
waxy appearance usually yellow discolouration often shins occassionally ulcerates and scars
107
Describe sclerodema
``` feels a bit like orange peel surface can be dimpled inflammatory - warm blanching shoulder - shawl distribution ```
108
Describe diabetic ulcers
``` foot ulcers - neuropathic over pressure points on feet venous ulcers- multifactorial peripheral vascular disease venous eczema ```
109
Describe granuloma annulare
round backs of hands and feet if widespread check for diabetes
110
What skin changes can be as a result of cushings / steroid excess?
acne striae erythema gynaecomastia
111
What skin changes can be seen in addisons?
hyper pigmentation | acanthosis nigracans
112
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
113
What skin changes can excess testosterone lead to and how is this caused?
``` acne hirsutism PCOS testicular tumours testosterone drug therapy ```
114
What skin changes can excess progesterone lead to and how is this caused?
acne dermatitis congenital adrenal hyperplasia contraceptive treatment
115
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 ```
116
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
117
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
118
Describe acanthosis nigricans
smooth, velvet like, hyperkeratotic plaques in intertriginous areas type 1 - malignancy type 2 - familial type 3 - obesity and insulin resistance
119
Describe vitamin B 6 deficiencies
pyridoxine | dermatitis
120
Describe vitamin B 12 deficiencies
cobalamin | angular chelitis
121
Describe vitamin B 3 deficiencies
niacin | pellagra (dementia, dermatitis, diarrhoea)
122
Describe zinc deficiency
``` acrodermatitis enteropathica inherited or acquired condition pustules, bull, scarring inherited alcoholism malabsorption states IBD bowel surgery ```
123
Describe vitamin C deficiency
``` punctate purpura / brusing corkscrew spiral curly hairs patchy hyperpigmentation dry skin dry hair non healing wounds inflamed gums ```
124
Describe erythema nodosum
``` streptococcal infection pregnancy / oral contraceptive sacrcoidosis drug induced bacterial / viral infection others ```
125
Describe pyoderma gangrenosum
ulcer with purple overhanging | associated with IBD, RA, myeloma
126
What types of drug reactions are there?
``` maculopapular urticaria morbilliform papulosquamous photo-toxic pustular lichenoid fixed drug rash bullous itch ```
127
What drugs commonly cause acute rashes?
``` antibiotics NSAIDs chemotherapeutic agents psychotropic anti-epileptic - lamitrigine, carbamazepine cardiac ```
128
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
129
Give examples of blistering disorders
``` drug induced - steven johnson syndrome toxic epidermal necrolysis immunobullous diseases bullous pemphigoid bullous pemphigus ```
130
Describe toxic epidermal necrolysis (TEN)
``` dermatological emergency majority drug induced most severe mucous membrane involvement stop suspect drug fluid balance SCORTEN severity scale ```
131
describe eryhtema multiforme
``` self limiting allergic reaction HSV, EBV, occasionally drug no or mild prodromme target lesions never progresses to TEN ```
132
What is the difference between bullous pemphigoid and pemphigus vulgaris
pemphigoid is deep | pemphigus is superficial
133
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
134
What is the treatment of dermatitis herpetiformis?
topical steroids gluten free diet oral dapsone
135
Describe urticaria
``` itchy, wheals lesions last <24 hours non-scarring common acute <6 weeks chronic >6 weeks immune mediated type 1 allergic IgE response ```
136
What is the treatment of urticaria?
antihistamines steroids immunosuppresion omilizumab
137
Describe erythroderma
``` descriptive term >80% involvement erythema psoriasis eczema cutaneous lymphoma drug reaction treat underlying skin disorders ```

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