Clinical Flashcards
1
Q
What is a macule?
A
hyperpigmented flat lesion which is <1cm
2
Q
what is a patch?
A
hyperpigmented flat lesion which is >1cm
3
Q
what is a papule?
A
raised well defined lesion which <0.5cm
4
Q
what is a nodule?
A
raised well defined lesion which >0.5cm
5
Q
what is a plaque?
A
raised flat top lesions that grow horizontal which is > 1cm
6
Q
what is a wheal?
A
a raised compressible dermal swelling
7
Q
what is a vesicle?
A
a fluid filled lesion <0.5 cm
8
Q
what is a bulla?
A
fluid filled lesion >0.5 cm
9
Q
what is a pustule?
A
pus filled lesion
10
Q
what is a cyst?
A
nodule with semi solid material
11
Q
what is an erosion?
A
superficial skin break in the epidermis
12
Q
what is an ulcer?
A
deep skin break down to the dermis
13
Q
what is a fissure?
A
linear split in the epidermis
14
Q
what is lichenification?
A
increased appearance of skin markings
15
Q
what is atrophy?
A
loss of epidermis +/- dermis
surface remains in tact
16
Q
what is scale?
A
accumulated fragments of keratin layer
17
Q
what is crust?
A
dried exudate
18
Q
what is a scar?
A
normal tissue replaced by fibrous tissue
19
Q
what are the characteristics of hypopigmented rashes?
A
paler - lack melanin
20
Q
what are the characteristics of hyperpigmented rashes?
A
increased melanin
contain hemosiderin
direct chemical staining
21
Q
what is psoriasis?
A
a chronic inflammatory skin condition characterised by scaly erythematous plaques, which typically follows a relapsing course
22
Q
what is the pathogenesis of psoriasis?
A
epidermis in psoriatic plaques is hyperproliferative. there is proliferation and dilation of blood vessels in the dermis and infiltration of inflammatory cells
23
Q
what are “trigger” factors associated with psoriasis?
A
streptococcus infection
stress
skin trauma (Koebener phenomenon)
alcohol
obesity
smoking
drugs: lithium, NSAIDs, beta blockers , antimalarials and sudden oral or potent topical corticosteroid withdrawal
24
Q
what types of psoriasis are there?
A
- Pustular psoriasis
may be generalized or localized.
Generalised pustular psoriasis (a potentially life-threatening medical emergency)
Rapidly developing widespread erythema, followed by the eruption of white, sterile non-follicular pustules which coalesce to form large lakes of pus.
Lesions associated with systemic illness, such as fever, malaise, tachycardia, weight loss, and arthralgia.
Usually presents in people with existing or previous chronic plaque psoriasis, but can also occur in people without a history of psoriasis.
Localized (palmoplantar) pustular psoriasis
Lesions on the palms and soles, such as yellow-brown pustules within established psoriasis plaques, or redness, scaling, and pustules at the tips of the fingers and toes.
2.Erythrodermic psoriasis
Erythrodermic psoriasis is a potentially life-threatening medical emergency.
Diffuse, widespread severe psoriasis that affects more than 90% of the body surface area
It can develop gradually from chronic plaque psoriasis or appear abruptly, even in people with mild psoriasis
Lesions may feel warm, and may be associated with systemic illness, such as fever, malaise, tachycardia, lymphadenopathy, and peripheral oedema
3.Chronic plaque psoriasis (psoriasis vulgaris)
most common type
Monomorphic, erythematous plaques covered by adherent silvery-white scale, usually on the scalp, behind the ears, trunk, buttocks, periumbilical area, and extensor surfaces (such as forearms, shins, elbows, and knees).
Lesions which are typically distributed symmetrically and can coalesce to form larger lesions.
- Scalp psoriasis
affects 75–90% of people with psoriasis.
It typically presents as chronic plaque psoriasis affecting the scalp area.
The whole scalp can be affected, or individual plaques may be visible. Plaques may be very thick, particularly in the occipital region.
5.Facial psoriasis
Well-demarcated plaques on the face, similar to those of chronic plaque psoriasis.
Lesions which may affect the hairline.
Possible mild scaling around the eyebrows and nasolabial folds, which may be due to co-existent seborrhoeic dermatitis (so-called ‘sebo-psoriasis’)
6.Flexural psoriasis
Itchy psoriasis lesions affecting areas such as the groin, genital area, axillae, inframammary folds, abdominal folds, sacral and gluteal cleft.
The elderly, immobile, and people who are overweight or obese are at increased risk of being affected
Lesions of chronic plaque psoriasis which are well-defined, but there may be little or no scaling, due to friction and occlusion at these sites.
Lesions are often red and glazed in appearance, and there may be a fissure in the skin crease.
7.Guttate psoriasis
Small, scattered, round or oval (2 mm to 1 cm in diameter) scaly papules, which may be pink or red.
Multiple lesions which may occur all over the body over a period of 1–7 days, particularly on the trunk and proximal limbs. Lesions may occur on the face, ears, and scalp, but rarely affect the soles of the feet.
A first presentation of psoriasis (classically after acute streptococcal upper respiratory tract infection), or as an acute exacerbation of plaque psoriasis.
8.Nail psoriasis
Nail psoriasis more commonly affects fingernails than toenails and may affect all parts of the nail and surrounding structures.
Nail changes can occur with any type of psoriasis, and are particularly common in people with psoriatic arthritis (up to 90% of people are affected). The incidence of nail involvement increases with the duration of psoriasis.
Nail pitting (depressions in the nail plate) is the most common finding.
Discolouration (for example the ‘oil drop sign’) — orange-yellow discolouration of the nail bed.
Subungual hyperkeratosis — hyperproliferation of the nail bed, with accumulation of keratinocytes under the nail.
Onycholysis — detachment of the nail from the nail bed, which may allow bacteria and fungi to enter and cause infection.
25
what other conditions can also develop due to psoriasis?
a seronegative arthropathy:
1. asymmetrical mono/oligoarthritic
2. symmetrical polyarthritis
3. psoriatic spondylitis
4. distal predominant
5. arthritis mutilans
26
how do you manage psoriasis?
1. education
2. Topical treatments:
vitamin D analogues: first line topical therapy e.g. calcipotriol
emollients: should be used liberally by all patients. greasy ointments such as olive oil may need to used on the scalp
diathranol: used in short contact regimens for stable chronic plaque disease as it burns and stains normal skin
coal tar: only used as in patient due to smell and mess
steroids: mild steroids are used flexural and palmar plantar disease
salicylate - is used to break down particularly hyper keratotic skin
n. b. Dovobet - gel which contains both calcipotriol and betamethasone dipropionate
3. phototherapy: most suitable for guttate (first line) or plaque psoriasis. best for more severe disease. can use UVB or PUVA.
PUVA more suitable for extensive large plaque psoriasis or localised pustular
4. Pharmacological
can also give drugs for more severe or non responsive
Methotrexate, Ciclosporin or aciterin
biological drugs: inhibit T cell activation and function or neutralise cytokines
first line: ustekinumab, adalimab, secukinumab
27
what is dermatitis (acute eczema)?
condition which causes a rash with inflamed red skin that is poorly demarcated and less scaly than psoriasis.
the barrier function of the pidermis is abnormal and skin is easily irritated
it is itchy
28
what is the clinical presentation of dermatitis?
essentially:
itchy, ill-defined, erythematous and scaly
29
give examples of endogenous dermatitis:
Atopic
seborrheic
varicose
discoid
30
give examples of exogenous dermatitis:
contact allergic
contact irritant
31
state the pathogenesis and histology for the following types of dermatitis:
contact allergic
contact irritant
atopic
drug-related
photo-induced
lichen simplex
stasis dermatitis
Pathogenesis histology
1. delayed type 4 reaction spongiotic dermatitis
2. Trauma e.g. soap and water spongiotic dermatitis
3. Genetic and environmental factors spongiotic dermatitis
4. Type 1 or 4 spongiotic dermatitis & eosinophils
5. Reaction to UV light spongiotic dermatitis
6. physical trauma e.g. scratching spongiotic dermatitis & external trauma
7. physical trauma - hydrostatic pressure spongiotic dermatitis & extravasation of RBCs
32
what are the causes of atopic eczema/dermatitis?
Genetic: family history of atopy is common . include mutations in the filaggrin protein which is a protein involved in maintaining the waterproof
infection: staph colonise lesions
allergens: difficult to avoid
33
how do you diagnose atopic eczema?
child must have itchy skin and 3 or more of the following factors:
1. onset before 2 years old
2. past flexural involvement
3. history of dry skin
4. personal history of other atopy ( or first degree relative if under 4 year old)
5. visible flexural dermatitis
34
what are the chronic changes of atopic eczema?
lichenification - chronic thickening and increased marking of the skin caused by scratching
excoriation - scratch marks self induced, often due to itching
secondary infection: crusting indicated staph aureus
35
what is the rash distribution of atopic dermatitis?
infants: face and scalp extensor surfaces involved, flexor surfaces and napkin area spared
children & adults: flexor surfaces, especially the wrist, cubital fossa, popliteal fossa and ankles
36
how do you manage atopic dermatitis?
DANGER : manage any severe weeping rash around the mouth: this could be eczema herpeticum which can be fatal
atopic eczema treatment in general:
1. Emollients and soap substitutes: dry skin itches and is susceptible to irritants. Use emollients liberally even when eczema is less active
2. anti histamine for pruritus e.g. hydroxyzine
3. topical corticosteroids:
mild: hydrocortisone
moderate: betnovate, eumovate
potent: betnovate, elocon
very potent: dermovate, etrivex
4. phototherapy mainly UVB
5. systemic immunosuppressants
6. biological agents
37
what is seborrheic dermatitis?
common inflammatory skin condition occurring in areas rich in sebaceous glands (such as the scalp, nasolabial folds, eyebrows, and chest). In infants the scalp is most commonly affected ('cradle cap').
38
what is the cause of seborrheic dermatitis?
over-growth of skin yeasts (malassezia)
also associated with immunosuppression - severe if HIV +ve or if patient uses drugs e.g. ciclosporin
39
what is the clinical presentation of seborrheic dermaititis?
adults and adolescent:
Red, itchy, scaly rash affects the following areas:
1. Scalp - mainly causes dandruff
2. Face - in particular the nasolabial nodes, behind the ear, eyebrows and cheeks
3. upper chest and back
4. Flexures and skin folds
child:
1. cradle cap
2. face
3. ears
4. neck
40
how do you manage seborrheic dermatitis
Infantile cradle cap: emollients +/- topical steroids
Adults: emollients + topical steroids + topical antifungal (ketoconazole) - if non responsive or more wide spread, oral antifungal can be given (daktacort or ketoconazole)
41
what does hyperkeratosis mean?
increased thickness of keratin layer
42
What does parakeratosis mean?
persistence of nuclei in the keratin layer
43
What does acanthosis?
increased thickness of epidermis
44
what is spongiosis?
oedema between keratinocytes
45
what types of contact dermatitis are there?
contact irritant -- non specific physical irritation
contact allergic - specific allergic reaction
46
give example of allergens which cause contact allergic dermatitis.
cosmetic ingredients – such as preservatives, fragrances, hair dye and nail varnish hardeners
metals – such as nickel or cobalt in jewellery
some topical medicines (medicines applied directly to the skin) – including topical corticosteroids, in rare cases
rubber – including latex, a type of naturally occurring rubber
textiles – particularly the dyes and resins that are contained in them
strong glues – such as epoxy resin adhesives
plants – such as chrysanthemums, sunflowers, daffodils, tulips and primula
47
what is the pathogenesis of contact allergic dermatitis?
1. Langerhans cell in epidermis process the antigen - this increases immunogenicity
2. processed antigen is then presented to Th cells in dermis
3. sensitised Th cells migrate into lymphatics and then to regional nodes where antigen presentation is amplified
4. on subsequent antigen challenge specifically sensitised T- cells proliferate and migrate to and infiltrate the skin
5. Rash and skin changes take 48-96 hours
48
How do you diagnose contact allergic dermatitis?
patch testing
49
how do you manage contact allergic dermatitis?
allergen avoidance
regular emollients
topical steroids during flares
50
what are the causes of contact irritant dermatitis?
soaps and detergents
antiseptics and antibacterial
perfumes and preservatives in toiletries or cosmetics
solvents
oils used in machines
disinfectants
acids and alkalis
cement
powders, dust and soil
water – especially hard, chalky water or heavily chlorinated water
plants – such as Ranunculus, spurge, Boraginaceae and mustards
51
give examples of professions which are more at risk from irritant contact dermatitis?
agricultural workers
beauticians and hairdressers
chemical workers
cleaners
construction workers
cooks and caterers
metal and electronics workers
health and social care workers
machine operators
mechanics and vehicle assemblers
52
what is acne vulgaris?
Acne vulgaris is a chronic inflammatory skin condition affecting mainly the face (99% of cases), back (60% of cases) and chest (15% of cases).
is characterised by blockage and inflammation of the pilosebaceous unit
53
what is the pathogenesis of acne vulgaris?
1. sebum produced by sebaceous gland plugs pilosebaceous unit
2. keratin and sebum build up to produce comedones (blackheads/whiteheads). basal kertinocyte proliferation in pilosebaceous follicles caused by androgen and corticotropin release hormones
3. Rupture causes acute inflammation ( caused by colonisation of Propionibacterium acne) + foreign body granulomas
54
what is the clinical presentation of acne vulgaris?
face, chest and upper back are most affected areas
Non-inflammatory lesions (comedones) which may be open (blackheads) or closed (whiteheads).
Inflammatory lesions such as:
Papules and pustules – superficial raised lesions
Nodules or cysts- deeper, palpable lesions which are often painful and may be fluctuant.
may also have scars
55
what are the risk factors of acne vulgaris?
Age 12-24
greasy skin
endocrine disorders - Hyper androgenism
56
how do you classify acne vulgaris?
Mild acne - mainly facial comedones
moderate acne - inflammatory lesions (papules and pustules) dominate, affecting face +/- torso
severe acne - nodules, cysts scars and inflammatory papules and pustules
57
how do you manage acne vulgaris?
mild acne:
topical benzoyl peroxide or topical retinoid
if poorly tolerated try azelaic acid
Moderate acne:
oral antibiotic combined with topical benzoyl peroxide or topical retinoid
contraceptive pill can be used in women
severe acne:
topical therapies and isotretinoin
58
what is rosacea?
a chronic relapsing/remitting disorder of blood vessels and pilosebaceous units in central facial areas typically in fair skinned people.
59
what is the clinical presentation of rosacea?
more common in women
pre-rosacea features:
1. flushing triggered by stress, alcohol, spices and sunlight
Rosacea signs and symptoms:
central facial rash with:
1. erythema
2. telangiectasia
3. papules and pustules
4. inflammatory nodules +/- facial lymphoedema
5. men have risk of rhinophyma ( swelling + soft tissue overgrowth of the nose)
6. ocular rosacea - conjunctivitis/blepharitis
60
how do you manage rosacea?
Use soap substitutes and avoid sun overexposure
1. topical metronidazole
2. topical therapies + oral antibiotics (doxycycline)
3. Isotretinoin - causes dry skin and lips and photosensitivity
4. talangectasia + rhinopyma: laser therapy
61
What is bullous pemphigoid?
the chief autoimmune blistering disorder in the elderly - due to IgG autoantibodies to the basement membrane
62
what are the signs and symptoms of bullous pemphigoid?
Patient is typically elderly
blisters are localised to one area, or widely spread on the trunk and proximal limbs
can have large tense bullae on normal skin on erythematous base
blisters burst to leave erosions but are non scarring
itchy erythematous plaques and papules may be presenting feature
A history of itch in the months preceding the onset of blistering
63
How do you diagnose Bullous pemphigoid?
Immunofluorescence +ve - Linear IgG and C3 along the basement membrane
skin biopsy: sub epidermal blisters + inflammatory infiltrates within blisters
Nikolsky sign negative
64
how do you manage bullous pemphigoid?
very potent topical steroids applied to lesions (prednisolone) - slowly reduced over 4 weeks
tetracycline antibiotics - steroid sparing agents better than oral steroids
65
what are the main causes of bullous (blistering) diseases?
infection (e.g. herpes)
insect bite
friction
eczema
drugs (e.g. ACE or furosemide)
66
Name the two main examples of bullous disorders.
Bullous Pemphigoid - split is deeper through DEJ
Pemphigus vulgaris - split is more superficial, intra-epidermal
67
what is pemphigus vulgaris?
a bullous disorder due to IgG antibodies against desmosomal components ( desmoglein 1&3) which leads to acantholytsis (keratinocytes separate from each other)
68
what is the clinical presentation of pemphigus vulgaris?
more common in younger people (<40)
typically affects scalp, face, axillae and groins
flaccid vesicles/bullae - thin roofed and leave eroded raw areas
lesions rupture to leave raw areas - increased infection risk
Mucosal involvement (eyes, genitals) : very common.
69
how do you diagnose pemphigus vulgaris?
Nikolsky sign positive
+ve immunofluorescence - intracellular IgG giving a crazy paving effect
skin biopsy of blisters
70
how do you manage pemphigus vulgaris?
prednisolone
steroid sparing agents: mycophenolate mofetil and azathioprine
use rituximab and IV immunoglobulin in resistant cases
71
what is nikolsky's sign?
top layers of the skin slip away from the lower layers when slightly rubbed
indicates plane of cleavage within the epidermis
72
what is dermatitis herpetiformis?
autoimmune skin condition caused by auto antibodies against tissue transglutaminase (TTG), which is the antibody implicated in coeliac disease and causes sub epidermal blisters in the skin
73
what is the clinical presentation of dermatitis herpetiformis?
small, intensely itchy blisters on an erythematous and swollen base.
itch can precede the blisters
lesions tend to be found on extensor aspects of elbows, forearms, knees, buttocks, scapulae, face and scalp. it is symmetrical
74
how do you diagnose dermatitis herpetiformis?
blood Anti TTG
biopsy: sub epidermal blisters with papillary micro abscesses
immunofluorescence: granular deposits of IgA within papillae of epidermis
75
how do you manage dermatitis herpetiformis?
Gluten free diet +/- dapsone
rare complication: increased risk of small bowel lymphoma
76
what is lichen Planus?
an inflammatory skin condition , characterized by an itchy, non-infectious rash on the arms and legs
77
what are the signs and symptoms of Lichen planus?
common with middle age
1. lesions are distributed at flexor aspect of wrists, forearms, ankles and legs
2. the lesions are described as:
1. purple
2. pruritic
3. poly-angular
4. planar (flat-topped)
5. papules
3. white lacy markings (Wickham's striae) found on papules and buccal mucosa
associated with Hep C
78
How do you manage Lichen planus?
symptomatic treatment
1. topical steroids are 1st line
2. oral steroids if extensive
can use emollients
phototherapy (UVB or PUVA)
79
what is tuberose sclerosis?
a multi-gene disorder which is autosomal dominant and effects virtually every organ system
80
what are the causes of tuberose sclerosis?
mutations on chromosomes 9q34 and 16p13.3
tumour suppressing genesTSC1 and TSC2 are the genes affected - code for hamartin and tuberin
81
what are the signs and symptoms of tuberose sclerosis?
skin:
ash leaf macules - oval shaped areas of hypopigmentation. earliest cutaneous sign of tuberose sclerosis
Periungal fibroma: fibroma's of the nail bed . they are small fleshy tumours which grow aroun and under the toenails or finger nails
sebaceous adenoma: angiofibroma of the sebaceous glands on the face
shagreen patches: leathery texture nodules and is found most commonly in the lower back region
other:
hamartomas - angiomyolipomas found on hear,lung and kidneys
bone cysts seen on x-ray
enamel pitting
82
what is Neurofibromatosis type 1?
an autosomal dominant genetic condition that causes tumours to grow along your nerves. The tumours are usually benign.
83
what are the sign and symptoms of neurofibromatosis type 1 ?
cafe au lait macules
neurofibromas
plexiform neuroma
axillary or inguinal freckling
optic glioma
2 or more lisch nodules on iris
a distinctive bony lesion
84
what are the 4 main subtypes of inflammatory skin diseases?
- spongiotic
- psoriasiform
- lichenoid
- vesiculobollous
85
what happens to the epidermis in psoriasiform inflammation?
acanthosis due to elongation of rete ridges
86
what happens in lichenoid inflammation?
basal layer damage
87
what happens in vesiculobullous inflammation?
blistering
88
what subtype of inflammatory skin disease does eczema, contact allergic dermatitis and photosensitivity come under?
spongiotic inflammation
89
what subtype of inflammatory skin disease does psoriasis come under?
psoriasiform inflammation
90
what subtype of inflammatory skin disease does lichen planus and lupus come under?
lichenoid inflammation
91
what subtype of inflammatory skin disease does pemphigoid pemphigus and dermatitis herpetiformis come under?
vesiculobullous inflammation
92
what type of nerve fibres transmit itch?
C fibres
| unmyelinated
93
what are salmon patches?
non vascular birthmarks found on the face or nuchal area
It is a central erythematous macule - majority will regress with time
94
what are port wine stains?
capillary malformations that are present at birth and are permanent
they are usually found in the head and neck region
the lesions are pink/red macule that is unilateral which tend to darken and thicken with age
location on the nerve is described in relation to the distribution of the trigeminal nerve
95
what is klippel-trenaunay syndrome?
rare congenital vascular disorder in which a limb may be affected by port wine stains, varicose veins, and bone and soft tissue growth
96
what is infantile haemangioma (strawberry naevi)?
benign vascular tumours that usually appears within the first month of life in the head or neck region
more common in females and premature babies
lesion: superficial, red plaque - majority undergo complete or partial resolution
97
where do melanocytes arise from?
neural crest
98
What are the three main types of skin cancers?
Basal cell carcinoma - most common
squamous cell carcinoma
Melanoma
99
what happens when melanoblasts settle in the skin?
ii. what is the normal melanocyte: basal keratinocyte?
they form melanocytes
ii. 1:5 - 1:10
100
what are the risk factors of malignant melanoma?
1. UV exposure
2. sunburn
3. fair complexion
4. many melanocytes or dysplastic naevi
5. +ve family history - MC1R defect leads to freckling
6. old age
7. had a previous melanoma
101
what are actinic lentigines?
also called 'age' or 'liver' spots
spots found on face, forearms and dorsal hands
related to UV exposure
these spots have an increase melanin and basal melanocytes
102
what are dysplastic naevi?
variegated pigment spots which are generally >6mm in dimeter
they are either sporadic (low risk of malignant melanoma) or familial (high risk of malignant melanoma)
103
what are the signs and signs and symptoms of malignant melanoma?
signs
ABCDEF:
Asymmetry in the outline of lesion
Border irregularity or blurring
Colour variation with shades of black, brown, blue or pink
Diameter >6mm
Evolution - all changing moles in size, elevation and/or colour are suspect
Funny looking mole - the lesion stands out
nodular melanomas: much more dangerous
Elevated
Firm
Growing
104
what types of malignant melanomas are there?
four main types:
1. superficial spreading (most common) - found on trunks and limbs it presents as a slowly enlarging pigmented lesion with colour variation and irregular border
2. Nodular - most aggressive type. rapid growing, varied sites but often trunk
3. Acral lentiginous - occur on the palms, soles and subungual areas
4. Lentigo maligna - arises within a lentigo maligna
105
how do you diagnose malignant melanomas?
Clinical
biopsy
check Breslow's thickness to determine prognosis:
the measurement of the depth of the melanoma from the granular layer of the epidermis down through to the deepest point of the tumour
106
how do you manage malignant melanomas?
initial:
primary excision to give clear margins (2mm)
sentinel node biopsy - if positive then do a regional lymphadenectomy
Main:
depends on assessment of Breslow :
1. if in-situ then clear by circa 5mm
2. if invasive but <1mm thick: 1 cm clearance
3. if invasive >1mm thick: 2 cm clearance
4. sentinel node biopsy if >1mm thick or thinner with mitoses
advanced treatment: difficult to manage
chemotherapy
immunotherapy
Genetic therapy
107
Give examples of epidermal tumour causing cancers.
1. Basal cell carcinoma (malignant)
2. squamous cell carcinoma (malignant)
3. Dysplasias-bowen's disease (pre-malignant)
4. Actinic keratosis (pre-maligant)
5. Viral lesions (pre-malignant)
6. seborrhoeic keratosis (benign)
108
what is seborrhoeic keratosis?
benign proliferation of epidermal keratinocytes
it is common on face and trunk and occurs usually in ageing skin
lesions: tuck on appearance - greasy hyperkeratotic surface. warty and rough
109
what is basal cell carcinoma?
it is the commonest skin cancer
best outcome for skin cancers
basal cells sprout from epidermis. the cells then invade the dermis, peripheral palisading.
slowly growing and locally destructive - never metastasises
110
what are the risk factors for basal cell carcinoma?
Fair skin
UV light exposure
intermittent sun damage during childhood
111
what are the three main types of BCC?
Nodular
superficial
infiltrative - most worrying
112
what is the clinical presentation of BCC?
Infiltrative:
prominent desmoplastic fibrous stroma
margins are poorly defined
may spread along nerves
Nodular:
pearly nodule with rolled telangiectatic edge on the face or a sun exposed site +/- central ulcer
causes local destruction if left untreated
Superficial:
lesions appear as red scaly plaques with raised smooth edge often on the trunk or shoulders
113
how do you diagnose BCC?
clinical presentation
biopsy
114
how do you manage BCC?
conservative: leave it and monitor
surgical :Excision (first line)
medical: topical imiquimod or fluorouracil - reasonable options for superficial lesion at low risk sites
can also do: cryotherapy, cutterage, radiotherapy, photodynamic therapy
115
What is squamous cell carcinoma?
second most common form of skin cancer
generally good prognosis
locally invasive
low but definite risk of metastasis
116
what are the main precursors for SCC?
1. Bowen's disease
2. Actinic keratosis
3. Viral lesions
all display squamous dysplasia
117
what is Bowen's disease?
it is SCC in SITU
118
what is the clinical presentation of Bowen's disease?
Scaly plaque that is well defined and has a flat edge and it slowly enlarges
Mainly presents in women on their lower leg
119
how do you manage Bowen's disease?
cryotherapy
topical fluorouracil or imiquimod
photodynamic therapy
curettage + cautery
120
what is actinic keratosis?
Pre malignant lesions associated with partial thickness intra-epidermal proliferation of atypical keratinocytes
121
what is clinical presentation of actinic Keratosis
lesions found on sun exposed area, especially somewhere on the head
lesions: pre-malignant crumbly yellow white scaly crusts
122
which virus are viral precursors of SCC associated with?
HPV
123
what are the riskfactors of SCC?
HPV
fair skin
cumulative sun damage over the years
immunosuppression
124
what is the clinical presentation of SCC?
Lesion:
ulcerated or crusted
firm and irregular
locally invasive can metastasise
seen on sun exposed sites (face, ears, dorsal hands)
can have chronic leg ulcers (uncommon)
can have xeroderma pigmentosum (rare)
sites with poorer prognosis:
scalp
ear
nose
125
how do you diagnose SCC?
biopsy
126
how do you manage SCC?
local complete excision in primary SCC
127
what does photosensitivity mean?
denotes conditions triggered by light
128
what are the two types of UV is the skin exposed to?
UVA - longer wave - penetrates glass
UBV - smaller wave length, main contributing type to sunburn and skin cancer
129
what is xeroderma pigmentosum?
group of autosomal recessive genetic disorders caused by deficiency in the DNA repairs mechanisms in the skin
130
what is the clinical presentation of xeroderma pigmentosum?
severe photosensitivity
accelerated photoaging
ocular damage
early formation of skin cancers
131
How do you manage xeroderma pigmentosum
patients required to undertake strict sun avoidance
most die in teenage years due to skin cancer
132
what is porphyria?
a group of cutaneous and systemic conditions associated with deficiency of enzyme involved in the synthesis of haem
133
what is porphyria cutanea tarda?
the most common type of porphyria
usually seen in middle aged men
commonly associated with liver disease - seen in patients often with haemochromatosis, hepatitis or alcohol misuse
134
what enzyme deficiency occurs with porphyria cutanea tarda?
Uroporphyrinogen decarboxylase -the porphyrin type accumulated is uroporphyrinogen 3
135
what is the rash of porphyria cutanea tarda?
ii. what other presentations are there?
blistering lesions on sun exposed sites that heal with scarring and are associated with hyper pigmentation
skin affected is fragile
ii. lot of hair growing on cheeks
136
how do you diagnose porphyria cutanea tarda?
bloods - porphyrin studies
woods lamp: urine shines pink instead of blue
137
what is acute intermittent porphyria?
form of porphyria where the enzyme deficiency is porphobilinogen deaminase. Therefore the porphyrin accumulated is porphobilinogen
commonly presents in females around the age of 30
138
what is erythropoietic protophopyria?
an autosomal dominant condition - most commonly seen in children
the enzyme deficiency is Ferrochelatase - leads to accumulation of the porphyrin: protoporphyrin IX
rash: sometimes no evidence of rash but there will be burning and itching on the skin with
139
what drugs can cause photosensitiviy?
NSAIDs
Diuetics
Amiodarone
Antibiotics: Tetracyclines, ciprofloxacin
140
what type of hypersensitivity reaction causes chronic actinic dermatitis?
type IV
141
what is the clinical presentation of chronic actinic dermatitis?
Most commonly seen in men over 50
develop eczematous type rash on sun exposed sites
often associated with contact allergic dermatitis
142
How do you manage chronic actinic dermatitis?
sun protection
standard eczema treatment of emollients and topical steroids
143
what is solar urticaria?
a photosensitivity condition where sunlight causes a Type I
144
what is the clinical presentation of solar urticaria?
immediate onset of erythema, urticaria and itchy rash upon exposure to sunlight
rash resolves in a few hours
145
how do you manage solar urticaria?
Sun avoidance
anti-histamines
146
what is urticaria (hives)?
a transient rash caused by oedema from mast cell degranulation and release of inflammatory mediators
147
what are the causes of urticaria?
1.Acute causes:
Allergy (most common cause for acute) - Type 1
Infections
parasites (helminths)
chemicals (insect bites, lates, drugs or food)
systemic disease
2.Chronic: urticaria which lasts more than >6 weeks
idiopathic
histamine releasing autoantibodies
3. Physical causes:
solar
cold
dermographism
cholinergic: after exercise or shower
autoimmune: SLE
148
what are the sign and symptoms of urticaria?
smooth, erythematous, itchy hives and wheals (localised swellings)
associated with angioedema
149
how do you diagnose urticaria?
skin prick test
Blood RAST tests
150
how do you manage urticaria?
Non sedating antihistamines
avoid allergen avoidance
UVB phototherapy - stabilises mast cells
151
when do angioedema develop?
oedema within the subcutaneous or sub mucosal tissues
152
what type of swelling does angioedema cause?
non pitting swelling
153
what is the the primary varicella zoster infection?
Chickenpox
154
how is chickenpox spread?
via droplets/vesicle fluid
incubation 11-21 days
155
what is the sign and symptoms of chickenpox?
crops of skin vesicles of different ages
often starts on face, scalp or trunk
the rash is more concentrated on the torso than the extremities
rash starts 2 days after infection - often starts on the back: macule - papuple to vesicle with a red surround leads to ulcers. crusting may then occur
156
how do you manage chickenpox?
Live attenuated vaccine for non-immune people and pregnant women
supportive - calamine lotion
if immunocompromised or on steroids give aciclovir
157
what is shingles?
also called herpes zoster
158
what is the pathophysiology of shingles?
following chicken pox, the varicella zoster virus can lay dormant in sensory nerve roots. Shingles is caused by reactivation of the dormant virus
159
what is the clinical presentation of shingles?
burning tingling pain and itch along dermatomal distribution which may preced rash
Rash: erythematous macules/ papules that develop into vesicles before crusting over and healing
160
what are the specific location of shingles?
ophthamlic (V1): reactivation of the virus in the trigeminal nerve. rash develops unilaterally over the forehead and around the eyes.
ramsay hunt syndrome: reactivation of the virus within the geniculate nucleus of the facial nerve. Rash and pain experienced in the auditory canal associated with:
Bell palsy
Deafness
Vertigo
Tinnitus
161
How do you manage shingles?
anti viral
if admission or immediate specialist advice is not indicated, consider the need for oral antiviral treatment (aciclovir, valaciclovir, or famciclovir).
pain management:
1. For adults with mild pain, offer a trial of paracetamol alone or in combination with codeine or a nonsteroidal anti-inflammatory drug (NSAID), such as ibuprofen.
2. Consider oral corticosteroids in the first 2 weeks following rash onset in immunocompetent adults with localized shingles if pain is severe, but only in combination with antiviral treatment.
162
What strains of herpes simplex are there?
Type 1: primary causes oral lesions but can Genital lesions
Type 2: only causes genital lesions
163
what is the clinical presentation of herpes simplex?
Rash: grouped painful, itch vesicles on an erythematous base that burst to form ulcers, crust over and then heal without scarring
oral: gingiva-stomatitis
additional symptoms: tingling, malaise, dysuria for genital lesions
can be acute or recurrent with recurrence happening due to virus laying dormant and not being eradicated with treatment
recurrent disease can present with erythema multiforme
164
give specific examples of herpes simplex?
Herpetic whitlow: inoculation of virus in the finger to produce a solitary painful lesion
Eczema Herpeticum: typically occurs in children with atopic eczema. Is a disseminated infection that presents with monomorphic, punched out lesions
165
how do you manage herpes simplex?
High dose acyclovir (oral or IV)
analgesia
education about spread
166
what does HPV cause?
Cervical cancer
warts: raised papules with a firm, roughened surface. Can also be described as papillomatous
167
what strains of HPV are there?
HPV 1-4: cause common warts
HPV 6/11: genital warts
HPV 16/18: cervical cancer
168
what is the management of HPV?
common: salicylic acid, cryotherapy and imiquimod
Genital: Podophyllin and imiquimod
169
what is the causative organism of molluscum contagiousum?
pox virus
170
what is the causative organism of erythema infectiosum?
Parvovirus B19 - can be detected by B19 IgM
171
what is the clinical presentation of molluscum contagiousum?
Self limiting viral infection seen in children, with lesions typically developing on head, neck and trunk
more commonly seen in those with atopic eczema
Rash: itchy, solid, pearly pink papules with umbilicated centre
172
what is the clinical presentation of erythema infectiosum?
self limiting infection, most commonly in children
Rash:
initially: bilateral macular erythema on cheeks
subsequent: maculopapular with lacy ertyhema on trunk and limbs
173
what is the causative organism of Orf?
parapox virus - found in sheep
174
what is the clinical presentation of Orf?
usually seen in farmers
Lesion: single, firm fleshy nodules on hand
Self limiting
175
what is the causative organism of Hand, foot and mouth disease?
coxsackie virus
176
what are the clinical presentation of Hand, foot and mouth disease?
Prodromal fever malaise
rash: grey vesicles surrounded by erythema and mouth ulcers
self limiting
177
what are the causative organisms of Dermatophyte infections?
Trichophyton rubrum – 70%. (only infects humans)
Trichophyton mentagraphytes – 20%.
Microsporum canid – rare.
178
what are dermatophyte infections?
fungal infections that invade and grow in dead keratin
spread is mainly indirect (man to man)
179
what are the sign and symptoms of dermatophyte infections?
lesion: round scaly itchy whose edge is inflamed than its centre
wet maceration in flexural areas
it is called tinea followed by the part affected:
1. Tinea capitis - scalp
2. Tinea barbae - beard
3. Tinea corpis - body
4. Tinea mannum - hand
5. Tinea unguium - nail
6. Tinea cruris - groin
7. Tinea pedis - foot: often only one foot involved
180
how do you diagnose dermatophyte infections?
skin scrapings from the active edge of a lesion or nail clippings
either used for microscopy or culture
181
how do you manage dermatophyte inefections?
Localised: topical antifungal e.g. terbinafine or imidazole creams twice daily for 2 weeks
Nails: difficult to treat - use terbinafine
toe nails is 3-6 months finger nails - 6-12 weeks
182
what is candida albicans?
a yeast infection
183
what are the signs and symptoms of candida albicans?
often pink and most satellite lesions
mainly affect the following areas:
1. mouth
2. vagina
3. glans of penis
4. skin folds (under breasts, groin areas, abdominal and nappy area in babies)
5. toe web
6. nail areas
184
how do you diagnose candida albicans?
swab for culture
oral candida wipes off with a spatula - unlike lichen planus
185
how do you manage candida albicans?
Skin: imidazole creams
mouth: Nystatin
vagina: imidazole cream +/- pessary
186
what is pityriasis versiocolor?
yeast infection caused by malassezia species
187
what is the clinical presentation of pityriasis versiocolor
hypopigmented or hyperpigmented scaly macules on the upper back trunk and back
risk factors:
living or staying in a warm, moist environment, including the UK, in the summer
sweating excessively (hyperhidrosis)
creams, dressings or clothing that do not allow your skin to breathe
being malnourished
having a weakened immune system
being a teenager or in your early 20s
188
how do you manage pityriasis versicolor?
imidazole cream for localised disease
antifungal shampoo
oral antifungals for resistant disease
189
what is impetigo?
contagious superficial skin infection caused by staph aureus (+/- strep pyogenes)
190
what is the clinical presentation of impetigo?
normally presents in ages 2-5
Lesions:
normally starts around nose and face
well defined lesions with honey-coloured crust on erythematous base (+/- superficial flaccid blisters)
191
how do you manage impetigo?
1st:topical fusidic acid for localised infection
severe: Flucloxacillin IV/PO (5-7 days)
Clarithromycin IV/PO if penicillin allergic
192
what is cellulitis?
acute infection of skin and soft tissues
193
what are the causes of cellulitis?
Beta haemolytic streps +/- staphs
194
what is erysipelas?
superficial form of cellulitis caused by strep pyogenes
usually affects the face and is a spreading rash with a fever
195
what is the clinical presentation of cellulitis?
Rash often seen on legs
signs:
pain
swelling
erythema
warmth
systemic upset
local lymphadenopathy
196
how do you manage cellulitis?
Flucloxacillin 1g qds (If penicillin allergic: Doxycycline 100mg bd PO)
severe: Iv flucloxacillin or vancomycin if allergic
197
what is scabies?
a highly contagious common disorder particularly affecting children and young adults
caused by sarcoptes scabei
198
How does scabies occur?
usually direct spread (person to person)
female mite digs a burrow and lays eggs which hatch as lave - the itch and rash is due to allergic sensitivity to the mite or its products
199
what is the clinical presentation of scabies?
very itchy papules, vesicles, pustules and nodules affecting finger-webs, wrist flexures, abdomen, buttocks and groins
itch is often worst at night
young infants: palms and soles are characteristically involved
Norwegian scabies: highly contagious which is normally seen in the elderly or immunocompromised
200
how do you manage scabies?
1st Permethrin - most effective topical agent
2nd choice: ,malathion - don't use if pregnant or <6months old
severe: oral ivermectin
201
what is the clinical presentation of head lice?
itch and papular rash on the nape (back of head)
lice can be visible
202
how do you manage headlice?
lotion options:
Malathion
Dimeticone
Isopropyl myristate
203
what is lyme diease?
a disease caused by a tick bite
the causative organism is Borrelia Burgdorferi
204
what is the clinical presentation of Lyme disease?
1. erythema chornicium migrans - annular erythematous lesions that looks like a bullseye. take 2 weeks to form after bite
2. systemic symptoms of malaise and arthralgia and firm bluish/red swelling on ears and nipples. occurs after 6 months
3. bluish discolouration and atrophy of the skin. systemic symptoms can be variable and include chronic pain
205
how do you diagnose lyme disease?
serology
206
how do you manage lyme disease?
remove tick
Doxycycline 100mg 2-3 weeks
amoxicillin 500mg TDS 2-3 weeks
207
what is the definition of a leg ulcer?
any break in the skin of the lower leg above the ankle
| which has been present for more than 4 weeks
208
what are the normal ranges of ABPI?
0.8 - 1.3
209
what ranges of ABPI show vascular disease?
less than 0.8
210
compare venous and arterial ulcer in terms of the border?
venous have a much more shallow edge/border
211
where do venous ulcers tend to develop?
around the malleoli
212
what are the 5 layers of the scalp?
```
Skin
Connective tissue
Aponeurosis
Loose connective tissue
Parietal bone
```
213
which skin condition is alopecia areata associated with?
atopic dermatitis
214
what is alopecia totoalis?
baldness effecting the whole scalp
215
what is alopecia universalis?
baldness effecting the whole body
216
what skin condition is behcet disease associated with?
erythema nodosum
other symptoms:
ophthalmic lesions e.g. uveitis and retinitis
recurrent painful genital ulcers
217
what is steven Johnston syndrome/ toxic epidermal necrolysis (TEN)?
conditions which are type IV hypersensitivity reactions characterised by necrosis and detachment of the epidermis
SJS is more mild than TEN
SJS only covers <10% of the body
TEN covers >30% of the body
218
what are the causes of SJS/TEN?
mainly drugs:
sulfonamides
antiepileptics
penicillins
cephalosporins
allopurinol
NSAIDs
trimoxazole
219
what are the signs and symptoms of SJS/TEN?
May have Flu like symptoms by skin involvement:
widespread painful dusky erythema
then necrosis of large sheets of epidermis
ulcerations - conjunctivae, oral cavity, labia and urethra
220
how do you diagnose SJS/TEN?
classified via SCORTEN score - measures extent of skin desquamation
221
how do you manage SJS/TEN?
* Cessation of causative drug.
* Supportive care.
* Emollients.
* Iv Ig.
222
what is erythema nodosum?
it is a pannicuitis and typically occurs on the shins and is raised in nature (nodular)
it is painful
it is associated with TB and sarcoidosis and IBD
chest radiograph can be used for diagnosis to exclude serious causes.
use NSAIDs for skin rash
223
what is erythema multiforme?
skin immune reaction which causes target lesions
first found on hands and feet and then limbs and trunk
fades over 2-4 weeks but recurrence is common
224
what condition are Kaposi sarcomas associated with?
AIDS
they are nodules, papules or macules which can be red, purple, brown or black
225
what is a rodent ulcer?
basal cell carcinoma
226
what is cutaneous larva migrans?
most common tropical dermatosis
caused by percutaneous penetration and subsequent migration of various nematode species
presentation: tupical snake like speriginous lesions
topical or oral thiobendazole is treatment of choice
227
what is hyperlipidaemia type 3 caused by?
mutation in the apo-E gene resulting in increased chylomicron remnants
228
A 3 year old boy presents on a sunny day in June. His mother reports he keeps crying and rubs at his skin when playing outside and this has been going on for a few weeks. His skin is sometimes a bit red, but there is never a rash and his skin is clear on examination now. He is skin type 1 with a few freckles evident, generally well, on no medication and there is no family history of skin problems?
Erythropoietic protoporphyria
229
what does the virulence factor cytotoxin leukocidin do?
ii. which bacteria is it associated with?
causing necrolytic skin infections by directly killing leukocytes
ii. staph aureus
230
State how the following four virulence act on the body :
Invasin
Adhesin
Aggressin
Modulin
Impedin
invasin → enables the organism to invade a host tissue,
Adhesin → enables binding of the organism to host tissue
Aggressin → causes damage to the host directly
Modulin → causes damage to the host indirectly
Impedin → enables the organism to avoid host defense mechanisms
231
what is skin failure?
loss of normal temperature control with inability to:
maintain the core body temperature
failure to prevent percutaneous loss of fluid, electrolytes and protein, with resulting imbalance
failure of the mechanical barrier to prevent penetration of foreign materials
232
Regarding topical steroids, which ONE of the following is TRUE?
Select one:
They have a vaso-dilatory effect
They cross the plasma membrane by endocytosis
They increase cell proliferation
They are lipophilic
Absorption is greater across hyperkeratotic than atrophic skin
lipophilic
233
Which of the following is a component of the strain of MRSA (Methicillin Resistant Staphylococcus Aureus) which causes severe skin infection such as necrotising fasciitis?
```
Select one:
Hyaluronidase
Coagulase
Protein A
Panton Valentine Leukocidin
Fibrinolysin
```
panton valentine leukocidin
234
Acute intermittent porphyria is due to impaired function of which enzyme?
Porphobilinogen deaminase
235
topical steroids are lipophilic true or false?
true
236
what type of infection are the following conditions:
Ring worm
Shingles
Head lice
Necrotising fasciitis
ring worm - fungal
shingles - viral
head lice - parasitic
necrotising fasciitis - bacterial
237
Describe the following topical treatments:
creams
Ointments
Lotions
Gels
Pastes
Creams → Semisolid emulsion of oil in water, contains preservative, cosmetically acceptable, non greasy
Ointments → Semisolid grease/oil, no preservative, less cosmetically attractive, greasy
Lotions → Liquid Formulation
Gels → Thickened aqueous solutions,
Pastes → Semisolids, stiff, greasy, difficult to apply, often used in cooling, drying, soothing bandages
238
how do you diagnose scabies?
Skin scrapings for microscopy
239
how do you diagnose impetigo?
Swab of lesion sent in bacterial container for microscopy and culture
240
how do you diagnose shingles?
Swab of lesion fluid sent in Viral container for PCR
241
how do you diagnose ringworm?
Skin scraping for microscopy and culture, and woods light
242
Which ONE of the following is true regarding topical therapies?
Select one:
A typical adult body requires 10g of ointment for one all over application
Creams are more likely than ointments to cause contact sensitisation
Ointments are more cosmetically acceptable to patients than creams
Occluding a treated area with clingfilm will reduce topical therapy penetration
Lotions are useful for very dry and hyperkeratotic eczema
Creams are more likely than ointments to cause contact sensitisation
243
what conditions make up the atopic triad?
hayfever
asthma
atopic eczema
244
The woman is a 20 year old waitress. She is already very conscious of her skin at work and does not want to have to put any greasy or smelly treatment on as it may show on her shirt.
Which of the following therapies would be best suited for her?
Select one:
Coal tar solution
Topical antibiotic gel
Very potent steroid ointment
Dithranol cream
Vitamin D analogue cream
vitamin D analogue
this is because:
Coal tar solution smells and can stain.
Topical antibiotics are not indicated as her condition is not caused by bacteria.
Very potent steroid ointment is not recommended due to the long term affects of steroid use.
Dithranol cream is a short contact therapy, time consuming to use and can stain.
Vitamin D analogue cream would be the 1st line treatment in her case as it is effective, easy to apply, non greasy and non-smelly.
245
what is "The disposition to judge things as being more likely, or frequently occurring, if they readily come to mind".
availability
246
what is "The tendency to perceptually lock onto salient features in the patient's initial presentation too early in the diagnostic process, and failing to adjust this initial impression in the light of later information".
anchoring
247
Which of the following statements are TRUE in patients with leg ulcers? (Must select ALL correct answers to gain marks)
Select one or more:
Ulcers can lead to malignant change
Contact sensitivity to topical treatments and bandages frequently develops
Systemic antibiotics are needed in all ulcers as
infection is inevitable
Compression bandages should be used to treat all ulcers that occur below the knee
Ankle exercises are important to maintain joint mobility with ulcers near the ankle
ankle exercises are important to maintain joint mobility with ulcers near the ankle
Ulcers can lead to malignant change
Contact sensitivity to topical treatments and bandages frequently develops
248
When excising skin, which of the following methods provides the best aesthetic result.
Select one:
An elliptical excision with the scalpel cutting at 45 degrees to the surface of the skin
An elliptical excision with the scalpel cutting at 90 degrees to the surface of the skin
A circular excision with the scalpel cutting at 90 degrees to the surface of the skin
A circular excision with the scalpel cutting at 45 degrees to the surface of the skin
An elliptical excision with the scalpel cutting at 90 degrees to the surface of the skin
249
Malignant melanomas can usually be effectively treated with combined therapy of chemotherapy and radiotherapy true or false?
false - Due to their embryological origins and the high amount of melanin within them, malignant melanomas do not respond well to chemotherapy or radiotherapy even when used in combination. The most effective treatment is early radical surgery
