Dermatology Flashcards
(303 cards)
1
Q
Type 1 hypersensitivity?
A
Immediate reaction
2
Q
Pathophysiology type 1 hypersensitivity?
A
- Activated TH2 cells release IL-4, IL-5, IL-13
- Cause B cells to release IgE
- IgE activates mast cells
- Mast cells release histamine, leukotrienes and cytokines
3
Q
Urticaria timeline?
A
Lesions appear within 1 hour + can last up to 24 hrs
4
Q
Angioedema?
A
Localised swelling of subcutaneous tissue (non-pitting, not itchy)
5
Q
Ix allergy? (4)
A
- RAST (IgE test)
- Skin prick
- Challenge test
- Serum mast cell tryptase level
6
Q
Tx allergy? (6)
A
Allergen avoidance, anti-histamine, corticosteroids, adrenaline, sodium cromoglycate, immunotherapy
7
Q
Adrenaline autoinjector?
A
For anaphylaxis
- 300 ug adults
- 150 ug children
8
Q
Type IV hypersensitivity?
A
Delayed (24-48 hrs), T cell mediated
9
Q
Ix type IV allergy?
A
Patch test
- Allergens prepared on Finn chambers
- Finn chambers placed on back and removed after 48 hrs
- Readings at 48 and 96 hrs
10
Q
Irritant contact dermatits?
A
Non-immunological process (irritants traumatise skin) e.g. nappy rash, lip-lick dermaitis
11
Q
Dermatitis tx? (6)
A
Allergen avoidance, emollients, topical steroids, UV phototherapy, immunosuppressants
12
Q
Epidermis composed of?
A
Stratified squamous epithlium
13
Q
Embryological origin of epidermis? Dermis?
A
Epidermis = ectoderm Dermis = mesoderm
14
Q
Melanocytes?
A
Pigment-producing cells from neural crest
15
Q
Layers of epidermis? (4)
A
Keratin layer, glandular layer, prickle cell layer, basal layer
(+ appendages = nail, hair, glands, mucosae)
16
Q
Blaschko’s lines?
A
Growth pattern of skin (does not follow nerves/lymphatics)
17
Q
How long does it take keratinocytes to migrate from basement membrane?
A
28 days
18
Q
Basal layer?
A
Small cuboidal, 1 cell thick
19
Q
Prickle cell layer?
A
Large polyhedral cells (lots of desmosomes)
20
Q
Granular layer?
A
ORIGIN OF CORNIFIED ENVELOPE (keratin layer)
2-3 layers of flatter cells
Contains: Lamellar (Odland) bodies, keratohyalin granules (contain filaggrin + involucrin)
21
Q
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.
What is the most likely diagnosis?
A
Erythropoietic protoporphyria
22
Q
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.
What is the most likely diagnosis?
A
Erythropoietic protoporphyria
23
Q
Skin problems make up what percentage of all general practice consultations?
A
~19%
24
Q
A 58 year old man presents in July with blisters on the dorsal aspect of his hands which have been appearing over the last few months, crust over and heal leaving scarring. He works as a joiner and is aware that his skin has also been more fragile than usual. You notice that he has a lot of hair growing on his cheeks. He is generally well and on no medication
What is the most likely diagnosis?
A
Porphyria cutanea tarda
25
Keratin layer?
Overlapping cell remnants (no nucleus)
| also contain lamellar bodies
26
What does HPV do?
Infects keratinocytes and causes warts
27
Where are melanocytes found?
Basal layer
28
Function of melancoytes
* Convert tyrosine to melanin pigment (Eumelanin = brown/black, Phaeomelanin = red/yellow)
* Pigment stored in melanosomes
* Melanosomes transferred to keratinocytes via DENDRITES
29
Vitiligo?
Autoimmune disease with loss of melanocytes
30
Albinism?
Genetic loss of pigment production
31
Nelson's syndrome?
Melanin-stimulating hormone produced in excess by pituitary
32
Langerhans cells?
Produced in bone marrow, found in prickle cell, dermis + lymph nodes
* ANTIGEN PRESENTING CELLS
33
Merkel cells?
MECHANORECEPTORS (sensation)
| * Present in BASAL cell layer
34
Merkel cell cancer?
Causes by virus, HIGH MORTALITY
35
Pilosebaceous unit?
Hair follicle + sebaceous gland
| hair receives pigment from melanocytes above dermal papilla
36
Phases of hair growth?
Anagen (growing), catagen (involuting), telogen (resting)
37
Excess androgen from tumour results in?
Virilisation
38
Alopecia areata?
Autoimmune hair loss
39
Nails grow how much?
0.1 mm per day
40
Where are stem cells for nail growth located?
Nail matrix (trauma can irreversibly affect nail growth)
41
Bullous pemphigoid?
Antibody attacks DEJ (dx = immunofluorescence)
42
Dermis composed of?
Ground substance, fibroblasts, macrophages, mast cells, lymphocytes, langerhans, collagen, muscles, blood vessels, lymphatics, nerves
43
Deep vascular plexus supplies?
| Superficial vascular plexus?
```
Deep = hair follicle
Superficial = LSA allowing diffusion of nutrients to epidermis
```
44
Pacinian corpuscles?
Deep pressure, found in dermis (onion rings)
45
Meissners corpuscles?
Vibration
46
Function of sebaceous glands?
Produce sebum
| * Controls moisture loss + protects against fungal infection
47
Apocrine glands?
Sweat glands in axilla and perineum (scent?)
48
Eccrine glands?
Sweat glands covering whole skin surface (esp. palms, feet, axilla)
49
Skin functions? (6)
Barrier, metabolism, thermoreg, immune defence, communication, sensory
50
Acute skin failure e.g.? Comps?
* Toxic epidermal necrolysis, erythroderma
| * Comps: dehydration, hypoalbuminaemia (protein loss), hypothermia, infection, disordered thyroxine metabolism, pain
51
Melanocyte:keratinocyte ratio?
1 melanocyte: 10 keratinocytes
52
Skin metabolism?
Vit D and thyroxine
* Vit D stored as hydroxycholecalciferol in liver, converted to 1,25 - dihydroxycholecalciferol in kidney
* Thyroxine -> thriiodothyronine (80% skin, 20% thyroid gland)
53
Eczema herpeticum?
Blindspot in immune system against herpes simplex virus
54
T lymphocytes found?
Both dermis and epidermis
* Epidermis = CD8
* Dermis = CD4 + CD8
55
T cells involved in systemic disease? (3)
* TH1 = psoriasis
* TH2 = atopic dermatitis
* TH17 = psoriasis + atopic dermatitis
56
Function of TH1 cells? TH2?
* TH1 = activate macrophages via IL2:IFNy
| * TH2 = help B cells make antibodies via IL4, IL5 and IL6
57
Dendritic cells found?
In dermis
* Dermal DC = Ag present
* Plasmacytoid DC = produce IFNa (found in diseased skin)
58
MHC?
Chromosome 6
* MHC class I = found on all cells, present endogenous Ag to CD8 cells
* MHC II = found on APC, present exogenous Ag to CD4 cells
59
Psoriasis Ax?
Triggered by environmental factors in genetically susceptible individuals
60
Pathology psoriasis?
* KC stimulate pDC to produce IFNa
* Release IL-1B/Il-6 and TNF
* Activate DC which activate TH1 and TH17
* T cells release IL-17/22
* Stimulates KC proliferation, AMP release, neutrophil-attracting chemokines
* Dermal fibroblasts release epidermal growth factors
61
Atopic eczema Ax?
Genetic + environment
62
Pathology atopic eczema?
Impairment in skin barrier + abnormal immune response
| impairment = mutations in fillagrin gene, decreased AMP in skin
63
Eczema lesions contain?
TH2, DC, KC, macrophages + mast cells
64
Primary immunodeficiency? Secondary?
* Primary = genetic
| * Secondary = acquired e.g. AIDS
65
Type I hypersensitvity? Type II? III? IV?
* I = IgE mediated
* II and III = IgG and IgM
* IV = TH1 cell
66
Effects of ageing on skin? (3)
Decreased ability to detect malignant cells, decreased ability to detect Ag (infection), decreased ability to distinguish self from non-self (autoimmunity)
67
Photodermatoses?
Skin disease caused by exposure to sunlight
68
Porphyria?
Group of diseases due to deficiency of enzymes needed to make haem
(haem needed to make haemoglobin, myoglobin, cytochromes, peroxidases, catalases)
69
Types of porphyrias? (3)
Porphyria cutanea tarda, erythropoetic protoporphyria, acue intermittent porphyria
70
Porphyria cutanea tarda?
Uroporphyrinogen decarboxylase deficiency
71
s/s porphyria cutanea tarda? (6)
Blisters, milia, hyperpigmentation, hypertrichosis, solar uricaria, morphoea
72
Ix porphyria cutanea tarda? (2)
Woods lamp, spectrophometer
73
Ax + Tx porphyria cutanea tarda?
* Ax: alcohol, viral hepatitis, oestrogens, haemochromatosis
| * Tx = underlying cause + symptoms
74
Erythropoietic protoporphyria?
Deficiency in ferrochelatase
| autosomal co-dominant inheritance
75
Ix erythropoietic protoporphyria?
RBC porphyrins, fluorocytes, transaminases, [Hb], biliary tract USS
76
S/s erythropoietic protoporphyria? (4)
redness, swelling, pain, itching
77
Mx and Tx erythropoietic protoporphyria?
Mx: 6 monthly LFTs and RBC prophyrins
Tx: visible light protection, prophylactic phototherapy, anti-oxidants (avoid iron)
78
Acute intermittent porphyria?
Deficiency of porphobilinogen deaminase
79
Types of allergic cutaneous drug eruptions? (4)
* Type 1 anaphylactic = urticaria
* Type II - pemphigus and pemphigoid
* Type III - purpura/rash
* Type IV - erythema/rash
80
Types of non-allergic cutaneous drug eruptions? (5)
* Eczema
* Psoriasis
* Phototoxicity
* Drug-induced alopecia
* Cheilitis, xerosis
81
Morphologies of cutaneous drug eruptions? (3)
| Presentation? (3)
* Exanthematous/morbiliform/mculopapular (75%)
* Urticarial (10%)
* Pustular/bullous
2
* Pigmentation, itch/pain, photosensitivity
82
When to suspect cutaneous drug eruptions?
Any patient taking medication who suddenly develops a symmetrical skin eruption (usually resolves when drug is withdrawn)
83
Risk factors for drug eruptions? (5)
* Young adults
* Female
* Genetics
* Virus/lupus
* Immunosuppression
84
Risk factors for drugs involved in eruptions? (4)
* Chemistry (B lactams, NSAIDs, HMW, hapten-forming)
* Route (systemic)
* Dose
* Half-life
85
Exanthematous drug eruption?
* Most common (90%)
| * Type IV hypersensitvity (4-21 days after taking drug)
86
s/s exanthematous drug eruption? (3)
* Widespread symmetrical rash (mucous membranes spared)
* Prutitus (itch)
* Fever
87
Indicators of potentially severe exanthematous drug reaction? (7)
* Involvement of mucous membrane + face
* Facial erythema + oedema
* Fever >38.5
* Skin pain
* Blisters, purpura, necrosis
* Lymphadenopathy, arthlargia
* SOB/wheezing
88
Drugs associated with exanthematous eruptions? (6)
* Antibiotics, allopurinol, anti-epilecptics (carbamazepine), NSAIDs
89
Urticarial drug reactions?
* Type I immediate
| will blanche unlike purpura in exanthematous
90
Acute generalised exanthematous pustolsis (AGEP)? (3)
* Anibiotics, CALCIUM CHANNEL BLOCKERS, antimalarials
91
Drug-induced bullous pemphigoid? (3)
* ACE-I, penicillin, furosemide
92
Liner IgA disease?
Vancomycin = blistering rash in ring forms
93
Fixed drug eruptions?
Red, painful, well-demarcated round plaques
| ALWAYS OCCURS in exactly the same spot!!!
94
Drugs associated with fixed drug eruptions?
* Cyclines, paracetamol, NSAIDs, carbamazepine
95
Severe cutaneous adverse drug reactions? (4)
* Stevens-Johnson syndrome
* Toxic epidermal necrolysis
* DRESS
* AGEP
96
Phototoxic cutaneous drug reactions?
Non-immunological skin reaction - usually UVA
97
Drugs associated with phototoxicity? (6)
THIAZIDES, antibiotics, NSAIDs, amiodarone, chloropromazine, quinine
98
Skin prick test contraindicated in?
Type III and IV hypersensitivity as can cause SJS, TEN and DRESS
99
What infections/diseases can increase risk of drug eruptions? (4)
* Immunosuppression, virus, CF, lupus
100
Tx cutaneous drug eruptions? (3)
* Withdraw drug, topical corticosteroids, antihistamines (type I urticaria)
101
Creams?
| Features of creams? (4)
Semisolid emulsion of oil in water
* Contain emulsifier and preservative (antibac)
* High water content (cools + moisturises)
* Non-greasy
* Cosmetically acceptable
102
Ointments?
| Features of ointments? (3)
Semisolid grease/oil (soft paraffin)
* No preservative
* Occlusive + emolient
* Greasy (less cosmetically attractive)
103
Lotions?
| Tx?
Liquid forulation
| Treat scalp, hair-bearing areas
104
Gels?
| Tx?
Thickened aqueous solutions
| * Treat scalp, hair-bearing areas, face
105
Pastes?
| Tx?
Semisolids containing finely powdered ZNO
| Tx: used in soothing bandages
106
Foams?
| Advantage? (2)
Colloid with 2-3 phases
Advantage = increased penetration of active agents + can spread easily over large areas of skin without being greasy/oily
107
Emollients tx?
For dry/scaly conditions e.g/ eczema
| prescribe 300-500g weekly
108
Sodium laurel sulphate?
Strong irritant found in some shampoos/creams
109
Topical steroid effects? (3)
| Tx? (4)
* Vasoconstrictive, anti-inflam, anti-prolif
Tx
* Eczema
* Psoriasis
* Lichen planus
* Keloid scars
110
Calicneurin inhibitors?
NSAID e.g. tacrolimus, pimecrolimus
| avoids side effects of steroids
111
Antiviral agents used to treat? (3)
Herpes simplex - topical
Eczema herpeticum - oral antiviral
Herpes zoster - oral antiviral
112
Antipruritics? (4)
* Menthol, caspaicin, camphor/phenol, crotamiton (e.g. eurax)
113
Keratolytics?
Used to soften keratin e.g. warts, eczema, psoriasis, corns
114
Commensal skin bacteria? (3)
* Staph epidermidis
* Corynebacterium (diptheroids)
* Propionibacterium
115
Staph aureus culture? Coagulase neg staph?
* Staph aureus = golden
* Coagulase neg = white
(ONLY staph aureus is coagulase positive)
116
a-haemolytic strep? B-haemolytic? Non-haemolytic?
* a-haemolytic = strep pneumoniae, veridans
* B-haemolytic = GAS, group B, Group C
* Non-haemolytic = enterococcus (common cause of UTI)
117
Coagulase test for staph?
Latex agglutination
118
Tx staph aureus?
Fluclox
119
Tx MRSA? (5)
* Doxycycline
* Co-trimoxazole
* Clindamycin
* Vancomycin
* Linezolid
120
UTI infection in women of child-bearing age?
Staph. saprophyticus
121
Types of B-haemolytic strep? (2)
* Group A (throat, severe skin infections)
| * Group B (neonatal meningitis)
122
Diseases associated with strep pyogenes (GAS)? (5)
* Infected eczema, impetigo, cellulitis, erysipelas, necrotising fasciitis
123
Strep pyogenes (GAS) tx?
Penicillin
124
Necrotising fasciitis tx?
SURGERY + antibiotics
125
Types of necrotising fasciitis? (2)
* Type I - mixed anaerobes + coliforms (usually post-abdominal surgery)
* Type II - GAS
126
Dermatophyte (fungal) infection (ringworm)? (7)
* Tinea capitis - scalp
* Tinea barbae - beard
* Tinea corporis - body
* Tinea manuum - hand
* Tinea unguium - nails
* Tinea cruris - groin
* Tinea pedis - foot (athlete's foot)
127
Dermatophyte pathogenesis? (5)
* Hyphae spread in stratum corneum (infects keratinised tissue only)
* Increased epidermal turnover causes scaling
* Inflammatory response
* Hair follicles invaded
* Lesion grows outward and heals in centre giving ring appearance
128
Epidemiology dermatophyte infections? (3)
* Males > females
* Scalp ringworm mainly affects children
* Foot + groin ringworm mainly affects men
129
Dermatophyte organisms and transmission?
Trichophyton rubrum (most common!!) - human to human transmission
130
Dx dermatophyte infection? (2)
* Woods light
| * Skin scrapings/nail clippings
131
Dermatophyte infection tx? (3)
* Small areas of infected skin/nails = clotrimazole cream or amorolfine nail paint
* Severe skin/nail infection + scalp infections = oral terbinafine/itraconazole
* Candida = clotrimazole cream + oral fluconazole
132
Ax scabies?
* Sarcoptes scabiei (chronic crusted form is called "Norweigan scabies" - HIGHLY CONTAGIOUS
133
Tx scabies? (2)
* Malathion lotion
| * Benzyl benzoate (avoid in children)
134
Type of lice infestations?
* Pediculus capitis (head louse)
* Pediculus corporis (body louse)
* Phthirus pubis (pubic louse)
Tx = malathion
135
Patients who need single room isolation and contact precautions? (3)
* GAS infection
* MRSA
* Scabies
136
Features of psoriasis? (4)
* Commonest form is plaque psoriasis
* Symmetrical
* Common sites = extensors, scalp, sacrum, nails
* Sharply demarcated, scaly, erythematous plaques
137
Specific signs of psoriasis? (2)
* Koebner phenomenon - areas of skin trauma e.g. scar
| * Auspitz sign - removal of surface scale reveals tiny bleeding points
138
Other types of psoriasis (other than plaque)? (3)
* Guttate
* Palmoplantar pustular
* Erythrodermic or widespread pustular (rare)
139
Psoriatic nail disease? (4)
* Onycholysis
* Nail pitting
* Dystrophy
* Subungal hyperkeratosis
140
Psoriasis co-morbidities? (6)
* Arthritis
* Metabolic syndrome (hypertension/obesity)
* Crohn's
* Uveitis
* Cancer
* SEVERE psoriasis = 3 x increased risk of MI!!!
141
Psoriasis tx? (7)
* Vitamin D analogues (calcipotriol, calcitriol), coal tar, dithranol, steroid ointments, EMOLLIENTS, phototherapy, immunosuppression (methotrexate)
142
Acne vulgaris?
Chronic inflammatory disease of the pilosebaceous unit
143
Acne pathogenesis?
* Pore occluded
* Bacterial colonisation
* Dermal inflammation
* Increased sebum production
144
Acne vulgaris distribution? Morphology?
* Distribution: face, upper back, chest
| * Morphology: comedones (open = blackhead, closed = whitehead), cysts, pustules
145
Acne treatment?
* Topical: benzyl peroxide, retinoid, antibiotics
| * Systemic: antibiotics, isotretinoin
146
Rosacea distribution + epidemiology?
* ose, chin, cheeks, forehead
| * 30 – 60 years, male and female
147
Features of rosacea? (4)
* Papules, pustules and erythema with no comedones
(NOT a disease of the pilosebaceous unit)
* Prominent facial flushing exacerbated by sudden change in temperature, alcohol & spicy food
* Enlarged / unshapely nose – rhinophyma
* Conjunctivitis / gritty eyes
148
Rosacea tx?
* AVOID topical steroids
* Topical therapy: metronidazole, ivermectin (to reduce demodex mite?)
* Oral therapy: oral tetracycline, isotretinoin
* Laser for telangiectasia
149
Lichenoid eruptions? Types? (2)
Damage to basal epidermis
| * Types = lichen planus + lichenoid drug eruption
150
Lichen planus feautures? (5)
| Tx?
* pink/purple flat shiny papules
* volar wrists/ forearms, shins and ankles
* Wickham’s striae – whitish lines in papules
* Intensely itchy
(lasts 12- 18 months before burning out)
Treat symptoms - topical steroids (oral steroids if severe)
151
Difference between pephigus and bullous pemphigoid? (2)
* Bullous pemphigoiD –
split is Deeper, through DEJ.
* PemphiguS –
split more Superficial, intra-epidermal
Nikolsky's sign (top layers of skin slip away when rubbed)
* Bullous pemphigoid = negative
* Pemphigus = positive
152
Epidemiology + distribution bullous pemphigoid?
* Elderly patients
| * Localised to one area OR widepsread on trunk + proximal limbs
153
Feautures bullous pemphigoid? (6)
* large tense bullae
* blisters burst to leave erosions
* non scarring
* itchy erythematous plaques in early disease (blisters present later)
* Nikolsky sign negative
* No mucosal involvement
154
Pemphigus vulgaris distribution?
Scalp, face, axilla, groin
155
Features pemphigus vulgaris? (4)
* Thin roofed bullae
* Lesions rupture to leave raw areas (increased infection risk)
* Nikolsky sign positive
* Mucosal involvement (eyes, genitals)
156
Prognosis bullous pemphigoid + pemphigus?
* Pemphigus = high mortality if untreated
| * Bullous pemphigoid = much lower risk
157
Tx of bullous disease? (3)
* Topical: emollients, steroids
* Oral: steroids
If pemphigoid = tetracycline antibiotics
158
Melanocytes found?
At DEJ
159
Dermis composed of? (3)
* Type I and type III collagen
* Elastic fibres
* Ground substance (hyaluronic acid + chondroitin sulphate)
160
Layers of dermis? (2)
| Epidermal basement membrane?
* Papillary dermis = thin and lies just beneath epidermis
* Reticular dermis = thick (contains appendages)
* Epidermal basement membrane = composed of lamin + collagen IV
161
Hyperkeratosis? Parakeratosis? Acanthosis? Papillomatosis? Spongiosis?
* Hyperkeratosis = increased thickness of keratin layer
* Parakeratosis = nuclei in keratin layer (normally un-nucleated)
* Acanthosis - increased thickness of epithelium
* Papillomatosis = irregular epithelial thickening e.g. wart
* Spongiosis = oedema between prickle cells e.g. eczema
162
4 main classifications of inflammatory skin diseases?
* Spongiotic-intraepidermal oedema e.g. eczema
* Psoriasiform-elongation of the rete ridges e.g. psoriasis
* Lichenoid-basal layer damage e.g. lichen planus and lupus
* Vesiculobullous-blistering e.g. pemphigoid, pemphigus + dermatitis herpetiformis
163
Lichen planus histology? (4)
* Irregular sawtooth acanthosis
* Hypergranulosis and hyperkeratosis
* Dermal infiltrate of lymphocytes
* Basal damage with formation of cytoid bodies
164
Immunobullous disorders? Examples? (3)
Blisters are MAIN feature
| e.g. pemphigus, bullous pemphigoid, dermatitis herpetiformis
165
Pathology pemphigus vulgaris?
AUTOIMMUNE
* IgG antibodies made against desmoglein 3
* Destruction of desmosomes
* end result is ACANTHOLYSIS
166
Bullous pemphigoid pathophysiology?
* IgG attack hemidesmosomes (attach basal cells to basement membrane)
* NO ACANTHOLYSIS
167
Dx bullous pemphigoid?
* Immunflourescence shows liner IgG around BM
| always send EARLY lesions for histology - old lesions show re-epitelialisation mimicking pemphigus vulgaris
168
Dermatitis herpetiformis? Features? (4)
Autoimmune bullous disease
* Associated with coeliac
* Itchy symmetrical lesions
* Elbows, knees, buttocks
* HALLMARK is papillary dermal microabscesses (neutrophils in papillary dermis)
169
Neurophysiology of itch?
* Unmyelinated C fibres in skin sense itch
| * Sensation processed in forebrain then hypothalamus
170
Mediation of itch? (3)
* Chemical mediators: histaine, PGE2, IL-2
* Nerve transmkssion: unmyelinated C fibres
* CNS: opiates
171
Causes of itch? (4)
* Pruritoceptive: something in skin triggers itch
* Neuropathic: damage to nerves that causes itch
* Neurogenic: opiates etc
* Psychogenic: psychological causes
172
Example of neuropathic itch? Neurogenic?
* Neuropathic = MS
| * Neurogenic = opiates
173
Pruritus tx? (5)
* Sedative anti-histamines (non-sedative useless)
* Emollients
* Antidepressants
* Phototherapy
* Opiate antagonists/ondansetron (serotonin antagonist)
174
Acute vs chronic eczema?
* Acute: papulovesicular, erythema, oedema, ooze
| * Chronic: lichenification, increased scaling
175
Features of eczema? (4)
* Itchy, ill-defined, erythematous + scaly
176
Most common cause of contact allergic dermatitis?
Nickel
177
Why does acute eczema "weep"?
Spongiosis occurs so rapidly that fluid accumulates as blisters rather than oozes
178
Pathology contact allergic dermatitis?
* Langerhans cell in skin presents antigen to CD4 cell
* Type IV hypersensitivity (T cells sensitised)
* On subsequent antigen challenge, sensitised T cells infiltrate skin (DERMATITIS)
179
How to distinguish between nappy rash and fungal infection?
* Fungi preferentially chose flexures
| * In nappy rash, flexures are generally spared
180
Atopic eczema associated with? (3)
Other atopic diseases: asthma, allergic rhinitis, food allergy
181
Eczema distribution?
Flexures (+ neck & orbits)
182
Fissure beneath ear lobe?
Pathopneumonic to eczema!!!
183
Chronic changes atopic eczema? (3)
* Lichenification
* Exoriation
* Secondary infection
184
Crusting in eczema indicates?
Staph aureus
185
Eczema herpeticum?
* Herpes simplex virus
| * Monomorphic (same shape + size) punched-out lesions
186
UK diagnostic criteria for atopic eczema?
Itching + 3 or more of:
* Visible flexural rash (cheeks + extnsor surfaces in infants)
* History of flexural rash (cheeks + extensor surfaces in infants)
* Personal history of atopy (or first degree relative if under 4 y/o)
* Dry skin
* Onset before age 2
187
Tx eczema? (6)
* Emollients, avoid irritants, topical steroids, infection tx, phototherapy, immunusuppressants
188
Most important gene in eczema?
Filaggrin (controls skin barrier function)
189
Other types of dermatitis/eczema? (6)
* Discoid eczema
* Photosensitive eczema
* Stasis eczema
* Seborrhoeic dermatitis (cradle cap)
* Pompholyx eczema
* Lichen simplex
190
Features of stasis eczema? (3)
| Where does it occur?
* Hydrostatic pressure
* Oedema
* RBC extravasation
Often occurs along lateral malleolus (extending to calf)
191
Pompholyx eczema?
Spongiotic vesicles occur due to acute eruption of eczema
192
Lichen simplex?
Caused by scratching, will go away on its own (can be treated with potent topical steroids)
193
s/s tuberous sclerosis? (9)
* Infantile seizures
* Ash-leaf macule
* Periungal fibromata + longitudinal ridging
* Facial angiofibromas
* Hamartomas
* Bone cysts
* Shagreen patches
* Enamel pitting
* Cortical tubers
194
Tuberous sclerosis?
Genodermatoses (autosomal dominant)
195
What can cortical tubers in tuberous sclerosis lead to?
Epilepsy and mental impairment
196
Genetic pathology tuberous sclerosis?
* Autosomal dominant
* Chromosomes 9 (TSC1) OR 16 (TSC2)
* Code for tuberin and hamartin
197
Tx tuberous sclerosis?
* Topical rapamycin for angiofibromas
198
Types of epidermolysis bullosa? (3)
* Simplex - within epidermis
* Junctional - DEJ
* Dystrophic - within dermis (scarring)
199
Epidermolysis bullosa?
10 genes involved
200
Haploinsufficiency? Dominant negative? Gain of function? Complete loss of protein?
* Hapoinsufficiency = only 1 copy of gene working (reduced protein production)
* Dominant negative = expression of abnormal protein interferes with normal protein
* Gain of function - mutant protein gains new function
* Complete loss of protein - autosomal recessive, 2 faulty genes produce no protein
201
Features of neurofibromatosis type 1? (7)
* Cafe au lait macules
* Neurofibromas
* Plexiform neuroma
* Axillary/inguinal freckling
* Optic glioma
* >2 Lisch nodules
* Bony lesion
202
Filaggrin mutation associated with? (4)
* Ichthyosis vulgaris
* Eczema
* Hay fever
* Asthma
203
2 main types of skin cancer?
* Non-melanoma = BCC + SCC
| * Melanoma
204
Skin cancer prevalence?
1/3 of all cancers
205
SSC incidence in Scotland?
334% increase from 1990 to 2011
206
Melanoma mortality?
Only 6% of all skin cancers but 75% of skin cancer deaths!!
207
Epidemiology melanoma?
Most common cancer in 15-24 year olds
208
Why is early diagnosis essential for melanoma?
Much more likely to metastasise than keratinocyte skin cancers
209
ABCDE rule for melanoma?
```
A - asymmetry
B - border
C - colour
D - diameter
E - evolution
```
210
Non-melanoma skin cancers prevalence?
* 90-95% skin cancers
* BCC = 75%
* SCC = 20%
211
BCC vs SCC? (4)
BCC
* Slow growing lump or non-healing ulcer ("rodent ulcer")
* painless
* locally invasive (doesn’t spread)
SCC
* warty lump/ulcer
* sun-damaged skin
* grow faster, may be painful &/or bleed
* more likely to spread
212
Different types of BCC? (4)
* Plaque
* Nodular
* Morphoeic
* Pigmented
213
Causes majority of non-melanoma deaths?
SCC
214
Precursor lesions for SCC? (2)
* Actinic keratoses
| * Bowen's disease (carcinoma in situ)
215
Keratoacanthoma?
Self-resolving form of SCC
216
Cutaneous horn?
SCC can present as cutaneous horn
217
Sites of metastasis for SCC? (5)
* Ear
* Lips
* Scalp
* Lymph nodes
* Bone
218
Survival rate metastatic SCC?
5 ys SR = 25%
219
What are chronic ulcers/wounds at risk of?
Developing SCC
220
Xeroderma pigmentosum?
Defect in nucleotide excision repair gene
221
Gorlin's syndrome?
Naevoid basal cell carcinoma - autosomal dominant
*GENETIC PREDISPOSITION TO BCC!!!
222
EB with regards to skin cancer?
Dystrophic form likely to develop SCC
223
Risk factors for skin cancer? (3)
* Genetic
* Immunosuppression e.g. orga transplant recipients
* Environmental carcinogens
224
Hallmarks of cancer? (6)
* Sustaining proliferative signalling
* Evading growth suppressors
* Activating invasion and metastasis
* Enabling replicative immortality
* Inducing angiogenesis
* Resisting cell death
225
Oncogene? Proto-oncogene?
* Oncogene: positively regulates cell division (over-active) e.g. Ras
* Proto-oncogene: normal (not mutated) form of oncogene
226
Tumour suppressor?
Gene that negatively regulates cell division e.g. p53
227
What pigment is seen in people who burn easily?
Pheomelanin
228
Relevance of sun exposure to SCC? BCC? Melanoma?
* SCC = life-long cumulative exposure e.g. outdoor workers
| * Melanoma and BCC = intermittent burning episodes e.g. sunbed use
229
Childhood suburn + melanoma risk?
Childhood sunburn increases melanoma risk 4-fold (rather than just 2-fold)
230
Chemicals associated with NMSC? (4)
* Coal tar, soot, creosate, arsenic
231
Autoimmune conditions that increase skin cancer risk? (2)
* UC incresases MM by 20%
| * Crohns increases MM by 80%
232
How UVB causes skin cancer? UVA?
* UVB = causes direct DNA damage (1000 x more damaging than UVA when sun directly overhead)
* UVA = causes indirect oxidative damage
(UV-induced immunosuppression also plays a role in skin cancer)
233
DNA damage caused by UVB?
Pyrimidine dimer
* cyclobutane pyrimidine dimer (more common)
* pyrimidine-pyrimidone (more mutagenic)
Both are formed by covalent bonding between adjacent pyrimidines
234
Nucelotide excision repair? (4)
For damage caused by UVB
1. Recognition of damaged DNA
2. Cleavage of damaged DNA
3. DNA polymerase fills in gap using undamaged strand as a template
4. DNA ligase seals the ends
235
Indirect DNA damage by UVA?
* Oxidation of DNA bases, especially deoxyguanosine to form 8-oxo-deoxyguanosine
* 8-oxo-dG mispairs with deoxyadenosine rather than deoxycytosine
* C -> A POINT MUTATION
236
Base excision repair? (5)
For damage caused by UVA
1. Recognition
2. cleavage of the altered base by DNA glycosylase
3. Base-free DNA cleaved away by endonuclease
4. Single nucleotide gap filled by DNA polymerase β
5. DNA ligase seals the ends
237
UV-induced immunosuppression? (3)
* decreased Langerhans cells in the skin so reduced ability to present antigens
* T-reg cells with immune suppressive activity
* anti-inflammatory cytokines e.g. IL-10 by macrophages and keratinocytes
238
Mutation associated with BCC? Treatment developed as result?
```
PTCH1 mutation (activates hedgehog signalling)
* Tx: vismodegib (hedgehod inhibitor)
```
239
Mutation associated with melanoma? Treatment as result?
* Ras/raf/MAPK pathway (mostly B-Raf mutation)
| * Tx: tramatenib (target is MEK)
240
Problem with vemurafenib in treating melanoma?
* It is a B-Raf inhibitor
| Only works for a few months until patient develops resistance to it (so used in combination with trametinib)
241
Mutation associated with familial melanoma? (2)
* CDKN2A mutation - inhibits CDKN2A which normally prevents cells from replicating when they contain damaged DNA
* CDK4 (cyclin dependent kinase 4) = mutation accelerates cell cycle
242
Ipilimumab?
PDL1 inhibitor
243
Melanocytes formed from?
Melanoblasts which migrate from neural crest to skin
244
Melanocortin 1 receptor (MC1R)?
* Turns phaeomelanin (red hair) into eumelanin
* One defective copy of MC1R causes freckling
* 2 copies = red hair + freckles
245
Ephilides?
Freckles (patchy increase in melanin pigmentation after UV exposure)
246
Actinic lentigines?
Age/liver spots following UV exposure (found on face, arms, back of hands)
247
Types of melanocytic naevi (moles)? (6)
* Normal
* Congenital
* Dysplastic
* Blue
* Halo
* Spitz
248
Small congenital naevi? Medium? Risk with large lesions?
* small = <2cm
* medium = >2 but <20cm
* large = 10% increased risk melanoma
249
Why do children with leukaemia tend to have more moles?
Chemotherapy leadsto immunosuppression which has been linked to increased naevi
250
Naevus development? (3)
* Childhood = junctional naevus: clusters of melanocytes at DEJ
* Adolescence = compound naevus: groups of melanocytes in dermis + junction
* Adulthood = intradermal naevus: entirely dermal (no junction involvement)
251
Features of dysplastic naevi? (3)
* >6mm diameter
* Varied pigment
* Border asymmetry
252
2 types of dysplastic naevi?
* Sporadic - not inherited, 1-2 atypical naevi, risk of MM slightly increased
* Familial - inherited, high penetrance (CDKN2A mutation), lifetime risk of melanoma 100%
253
What distinguishes dysplastic naevi from melanoma?
Unlike melanoma, epidermis is not affected (can be mistaken for melanoma-in-situ)
254
Halo naevi?
Peripheral halo of depigmentation (lots of inflammatory lymphocytes)
255
Blue naevi?
Entirely dermal and consist of dendritic spindle cells (may mimic melanoma)
256
Spitz naevus?
Consist of large spindle/epitheloid cells (most are benign)
257
Features of Spitz naevus?
* Pink/red colour due to prominent vasculature
| * Epidermal hyperplasia
258
Epidemiology MM? (3)
* Female > male
* Middle-age
* Can arise de novo (majority) or from dysplastic naevi
259
Ax MM? (3)
* Sunburn early childhood
* UV exposure
* Genetic i.e. skin colour + dysplastic naevi
260
When to suspect melanoma? (6)
* Change in shape
* Bleeding
* Different colours
* Development of satellite nodules
* Ulceration
* New naevus in adulthood (naevi usually develop in childhood)
261
4 types of melanoma?
* Superficial spreading (commonest) - trunk and limbs
* Acral/mucosal lentiginous -acral and mucosal
* Lentigo maligna - sun damaged face/neck/scalp
* Nodular - often trunk
262
Why is nodular melanoma very dangerous?
It only has a vertical growth phase (no flat spreading growth phase) so suddenly appears as lump on skin
263
Melanoma prognosis?
Related to Breslow's thickness
* PpTis (in-situ) - 100% survival
* pT1 < 1mm - 90% survival
* pT2- 1-2mm - 80% survival
* pT3- 2-4mm - 55% survival
* pT4 > 4mm - 20% survival
264
Other adverse prognostic indicators (other than Breslow's thickness) for melanoma? (4)
* Ulceration (suffix is b e.g. pT3b)
* High mitotic rate
* Lymphovascular invasion
* Satellites
265
Melanoma tx? (4)
* Excision (if sentinel node involvement, lymphadenectomy)
* Chemo
* Acral melanomas have c-kit mutation so can be treated with imatinib
* BRAF inhibitor (vemurafenib) - only works for few months so paired with MEK inhibitor e.g. trametinib
266
Epidermal tumours other than melanoma? (4)
* Benign-seborrhoeic keratosis
* Precancerous = Bowen's, actinic keratosis, viral lesions
* BCC
* SCC
267
Seborrhoeic keratosis? Features? (3)
Benign proliferation of keratinocytes
* Common in ageing skin
* Found on face + trunk
* Stuck-on appearance
268
Leser trelat sign?
Eruption of many seborrhoeic keratoses - can be sign of cancer
269
3 types of BCC? (3)
* Nodular
* Superficial
* Infiltrative (morphoeic)
270
What is a chronic leg ulcer?
An open lesion between knee and ankle that remains unhealed for >4 weeks
271
What are most chronic leg ulcers?
Venous
272
Lipodermatosclerosis?
Sclerosis in response to venous hypertension
273
Features of venous ulcer vs arterial ulcer? (2)
* Venous = shallow
| * Arterial = very sharp edges, punched-out deep ulcer (clues = hairless, cold leg)
274
Features of Vasculitis? (4)
* Painful
* Sudden onset
* Purpuric rash
* Necrotic
275
Non-healing shallow, well-defined leg ulcer?
BCC
276
Ix chronic leg ulcer? (3)
* ABPI (establish if arterial disease)
* Wound swab (only if sign of infection)
* Bloods - FBC, LFTs, U + E, CRP
277
ABPI values?
* 1.0 = normal
* 0.8 - 1.3 = compress
* <0.8 = vascular disease
* >1.5 = calcification
278
Venous ulcer tx? (2)
* Non-adherent dressing + COMPRESSION (4 layer compression bandaging)
* Leg elevation
279
Slough? How can slough be removed? (3)
Bacteria, exudate
* Compression bandaging
* Hydrogels
* Manual debridement
280
Commonest site for venous leg ulcers?
medial and lateral malleoli
281
What shape are you aiming for when padding and shaping a leg prior to bandaging?
Cone
282
Tinea pedis tx?
ORAL terbinafine (as topical clotrimazole cannot properly penetrate nail)
283
Complication of facial shingles?
Ramsay Hunt syndrome (post-herpetic neuralgia)
284
When may BCC kill?
Very unlikely to metastasise + very slow growing so can only kill when invading something like eye ---> brain
285
Precursors SCC? (3)
* Bowen's (especially on legs)
* Actinic keratosis
* Viral lesions
286
Bowens disease? Epidemiology?
* SCC in-situ (no dermal invasion)
| * Usually older ladies' legs
287
Actinic keratosis?
Sun-exposed skin esp. scalp, face, hands
288
Viral precursors SCC?
* Viral genital lesions
* Eythroplasia of Queryat (penile bowen's)
Both associated with HPV
289
Virulence factor examples? (5)
* Adhesin – enables binding of the organism to host tissue
* Invasin – enables organism to invade host
* Impedin – enables organism to avoid immune system
* Aggressin – causes damage to host directly
* Modulin – induces damage to host indirectly
290
Dangerous conditions associated with staph aureus? (2)
Toxic shock and SSS
291
Staph aureus virulence factors? (5)
* Capsule
* Fibrinogen binding protein (adhesin)
* Coagulase (clots plasma)
* PVL (leukocidin)
* TSST-1 (shock)
292
Effects of TSST-1? (5)
Rapid (48 hrs)
* high fever
* vomiting
* diarrhoea
* sore throat
* myalgia
293
Staphylococcal food poisoning caused by? (3)
* SeA, SeB, SeC
294
Scalded skin syndrome caused by which staph aureus toxins? (2)
Exfoliatin toxins - often neonatal
| * ETA and ETB target desmoglein-1
295
what is significant about TSST-1 ?
it is a superantigen!!! Activates 1 in 5 Tcells (normal Ag 1:10,000)
* Cytokine storm
296
Toxic shock syndrome diagnostic criteria? (4)
* Fever
* Macular rash + desquamation
* Hypotension
* >3 organ systems involved
297
Severe skin infections associated with PVL? (3)
* Recurrent furunculosis
* Sepsis
* Necrotising fasciitis
298
CA-MRSA? Associated diseases? (2)
PVL + a toxin
* Necrotising pneumonia
* Severe contagious skin infections
299
Necrotising pneumonia?
Caused by CA-MRSA
* Flu like symptoms that progresses to ARDS DESPITE ANTIBIOTICS!!!!!!
300
GAS skin diseases? (3)
* Impetigo
* Cellulitis
* Necrotising fasciitis
301
Cellulitis?
Infection in dermis
302
SLS?
Streptolysin - a haemolysin
303
Toxic shock caused by? (2)
s.aureus (no bacteremia) OR s.pyogenes (invasive)
