Dermatology - Skin Cancer, Acne, Hair and Nails Flashcards
(322 cards)
1
Q
Classification of neoplasia
A
Benign and malignant
Melanoma and non-melanoma
According to origin
2
Q
Where do melanocytes arise from
A
Neuro-ectoderm
3
Q
Mitotic rate of melanocytes
A
Low mitotic rate
4
Q
Where can melanocytes in embryonal life be found
A
Diffusely in the dermis
Migration to final location is key
5
Q
By the end of gestation, dermal melanocytes disappear except for
A
Head and neck
Dorsal aspects of distal extremities - typical sites for dermal melanocytosis and melanocytomas (blue naevi)
Pre sacral
6
Q
What do ventral neural crest cells form (trunk NCCs)
A
Melanocytes
Neurons, glia of ganglia
Adrenal medulla
Schwann cells
7
Q
What do cranial neural crest cells
A
Melanocytes Neurons, glia of ganglia Dermis of head Smooth muscles Chondrocyte osteocyte
8
Q
Proportion of melanosomes in membrane bound packets in different races
A
11% for Africans
37% for Asians
85% for caucasians
9
Q
Melanocyte/ keratocyte unit
A
Melanocytes present in epithelium 1: 20-40 keratocytes
Melanin stays above the nucleus of basal keratocytes, like an umbrella
10
Q
How is melanin transferred
A
Transferred to epithelial cells via dendritic processes
11
Q
What is melanin proaction driven by
A
UV exposure through POMC and alpha-MSH
12
Q
Natural hx of nave
A
Simple lentigo –> junctional nevus –> compound naves –> intradermal naevus —> regressed naevus
13
Q
Lentigo
A
Pigmented, flat or slightly raised lesion, not caused by sun exposure
14
Q
Frequency of melanomas
A
3rd most frequent skin tumour
15
Q
ABCD of histology of melanomas
A
Asymmetry
Border irregularity
Conspicuous junctional activity
Dermal mitoses
16
Q
Major types of melanomas
A
Lentigo maligna (LMM)
Superficial spreading
Nodular
Acral-lentiginous
17
Q
Acral
A
Affecting peripheral parts of body e.g. limbs, ears etc
18
Q
What are melanoma lesions composed of
A
Melanocytes
19
Q
Growth phases of melanomas
A
Radial (horizontal)
(Micro) invasive radial
Vertical
20
Q
Sun damage/ area of LMM
A
Prominent
21
Q
Sun damage/ area of superficial spreading melanoma
A
Intermittent sun exposure areas
22
Q
Sun damage/ area of nodular melanoma
A
Anywhere, mainly intermittent
23
Q
Sun damage/ area of acral lentiginous melanoma
A
Variable
24
Q
Prognostic factors of melanoma
A
Breslow thickness Ulceration Mitotic rate Perineural/ Vascular invasion TILs
25
Dysplastic naevus
Abnormal but non-cancerous moles on the skin
26
How does UV rays act as a carcinogen
Inhibits DNA repair, apoptosis and cell signalling pathways that prevents skin cancers
27
Carcinogensis cycle in skin
UV
| DNA lesion --> mutation ---> gene ---> cell phenotype ---> clonal expansion ----> precancerous or carcinoma
28
How does UV trigger exposure differ between skin cancer
SCC --> flash fry (blistering burns)
| BCC --> intermittent simmer (frequently tanning/ burns)
29
What proportion of BCCs are found on busy sites w. intermittent sun exposure
1/3 e.g. trunk and legs
30
Does the incidence of SCCs or BCCs increase more quickly w/ UV dose
SCC
31
Do SCCs or BCCs occur later in life
SCCs
32
How is vitamin D acquired
From UV skin exposure and diet
| Calcitriol increases Ca levels
33
Risk factors for skin cancer
```
Skin types (Fitzpatrick I)
Sunburns (esp childhood)
Outdoor exposure - occupation (e..g builder)
Living in sunny location
Immunosuppressed
Sunbeds & sunbathing
Fhx
PMH of skin cancers
Genetic disorders e.g. albinism
```
34
Transplant pts and skin cancers
AK and SCC 10-20x increase in sun-exposed skin
Cancer develops due to imunosupression
SCCs are usually unaggressive
35
Relevant drugs given to transplant pts that have a relation w/ skin cancer
Cyclophosphamide, ciclosporin and azathioprine are mutagens when followed by UVA
36
Types of albinism
Occulocutaneous albinism
| Occular albinism
37
Types of occulocutaneous albinism
Type 1: more severe - no melanin
| Type 2: some melanin
38
Occular albinism
Normal, or slightly paler than normal for their ethnicity, skin and hair
39
Common cutaneous precancerous lesions that are UV induced
Actinic (solar) keratoses (AKs)
Bowen's disease (carcinoma in situ)
Lentigo maligna
PUVA keratoses
40
Common cutaneous precancerous lesions that are viral induced
Vulval intraepithelial neoplasms (VIN)
PIN (incl Bowenoid Papulosis)
AIN
41
Actinic keratoses
Solar keratoses
| Proliferations of cytologically aberrant epidermal keratinocytes
42
AK's and risk of skin cancer
Approx 1:100 to 1:1,000 risk of SCC per AK
| Strong predictor of development of melanoma or non-melanoma skin cancers
43
Risk factors for AKs
```
Individual - older age, M, Fair skin, blonde hair
Cumulative UV radiation exposure
Immunosuppresion
Prior hx of AKs of other skin cancers
V rare genetic disorders
```
44
Genetic disorders that are risk factors for AKs
Xeroderma pigmentosum
Bloom syndrome
Rothmund-Thomson syndrome
45
Clinical findings of AKs
Sun exposure body sites
Pruritus, brining orb stinging pain, bleeding and crusting
2-6mm erythematous, flat, rough or scaly papule
46
Arsenical keratoses (ArKs)
Associated w. c/c arsenicism
| From medicinal, occupational and environmental exposures
47
Common occupations for ArKs
```
Miners
Smelters
Agricultural
Computer microchip
Electroplating
Glassmkainhg
```
48
What are ArK's associated w/
Bowen's disease
BCC
SCC
Internal malignancies
Potential to develop into invasive SCC
49
Latent period of ArKs
40yrs
50
Aetiology and pathogenesis of ArKs
Arsenic reacts w/ -SH (sulfhydrl groups) in tissue proteins
| Chromosomal mutations and breaks occur in p53
51
Clinical findings of ArKs
2-10mm, punctuate, yellow, keratitis papules
Seen in palms and soles - thenar and lateral borders of the hands, side of fingers
Areas of constant pressure or repeated trauma
52
SCC in situ
Bowen's disease
Potential to progress to invasive SCC
Can be seen in genital mms (papilloma virus)
53
Epidemiology of SCC in situs
Rare in individuals younger than 30 years except on genitals
54
Bowen's aetiology and pathogenesis
UV exposure (sunlight and therapeutic)
Immunosuppression
Infection w/ HPV
C/c arsenicism
55
Clinical findings of Bowen's disease
```
Discrete, slowly enlarging
Pink to erythematous, thin plaque
Well-dermacated, irregular borders
Overlying scale or crust
Sun-exposed areas
```
56
Lentigo maligna
Subtype of melanoma in situ
Seen in chronically sun-expsoed areas e.g. cheeks, nose, neck, scalp and ears
Common in 7th and 8th decades
57
Pathogenesis of lentigo maligna
Cumulative sun exposure
58
LM vs LMM
Lentigo maligna may progress to Lentigo Maligna Melanoma w/ time
59
LM clinical findings
Flat, slowly enlarging brown, freckle-like macule
Irregular shape and offering shades of brown and tan
Ill-defined borders
60
What are BCCs derived from
Non-kertainising cells originating in the basal layer of the epidermis
61
Epidemiology of BCCs aka rodent ulcer
Most common cancer in humans
| Almost s common as all other others combined
62
Natural pathway of BCC
Untreates, will invade locally and compromised function and cosmoses
63
Metastasis in BCCs
Extremely rare
64
Risk factors for BCCs
```
UV exposure
Light/ red hair
Blue eyes
Northern European ancestry
Type 1 or 2 skin
Freckles
Fhx
```
65
Genetic causes of BCC
```
Gorlins syndrome (dental cysts and palm pits) - pITCH mutation
Xeroderma pigmentosum
```
66
Clinical px of BCCs
Intermittent bleeding
May appear to heal
Pearly, translucent, ulceration, telangiectasis
Rolled edge
67
BCC subtypes
```
Nodular BCCs
Pigmneted BCCs
Superficial BCCs
Morpheaform (sclerosing) BCCs
Fibroepithelium of Pinkus
```
68
Features of nodular BCC - most common
Translucent papule or nodule seen in sun-exposed areas
Usually, telangiectasia and rolled border
Large lesions have central necrosis (rodent ulcer)
69
Features of pigmented BCC
Subtype of nodular BCC
increased melaninisation --> hyperpigmented, translucent papule/ nodule
May be eroded
70
Features of superficial BCCs
Commonly on trunk
Erythematous patch
May resume eczema
71
When to suspect superficial BCC
Isolated patch of 'eczema' that doesn't respond to treatment
72
Features of morpheaform (scleroisng) BCC
Aggressive variant
Ivory-white appearance
May resemble a scar or morphea
73
When to suspect morpheaform BCC
Unexplained scars
74
Features of fibroepithelioma od pinkus
Pink plywood lesion, commonly on lower back
May be difficult to distinguish from a skin tag
V rare
75
What is a SCC
Malignant neoplasm derived fron suprabasal epidermal keratinocytes
Usually evolves from AKs or Bowen's disease
Clinical px variable
76
Predisposing factors for SCC
```
Precursor lesions, UV, immunosupression
Burns or long term heat exposure - Marjolin's syndrome
C/c scarring
Smoking
Some c/c infl dermatoses
Papillomavirus infection
Geno dermatoses
```
77
Geno dermatoses
Albinism
Xeroderma pigmentosum
Prokeratosis
Epidermolysis bulls
78
Clinical findings of SCC
Flesh-colour or erythematous
Hyperkertatotic, bleeding, oozing, crusting
Papule, nodule or plaque
79
What may SCC look like
May be pigmented or ulcerate (wet beefy appearnce)
May be cutaneous iron
May be verruccous (wart-like)
Rarely, like an abscess, particularly if in perifungal location
80
Commonest locations of cutaneous melanoma
Men - back
| Women - legs, then trunk
81
Risk factors for cutaneous melanoma
```
UV radiation exposure
Phenotypic characteristics
Hx of prior melanoma
Fhx of melanomas
Mutation in p16, BRAF or MCR1R
Xeroderma pigmentosum
```
82
Phenotypic characteristics as risk factors
Fair skin, tendency to sunburn or freckles
Blue/ green eyes
Red/ blonde hair
Numerous typical Nervi and/ or more than one typical naevus
Large congenital naevus
83
Subtypes of melanoma
Superficial spreading malignant melanoma (SSMM)
Nodular melanoma
LMM
Acral lentiginous melanoma
84
Features of SSMM
Most common sub-type
Most frequently the lower legs of women and upper back of men
Wide range of aprerance
Associated w/ pre-existing naevi
85
Epidemiology of SSMM
Most commonly 4th to 5 th decade on intermittently sun-exposed areas
Most common subtype of melanoma
86
Most common site of nodular melanoma
Trunk
| Typically, uniformly dark blue-black or bluish-red raised lesion
87
Common areas for LMM
Face
| Many have sub-clinical lateral growth so higher recurrence rates
88
Epidemiology of Acral Lentiginous Melanoma
2% of melanoma in Caucasian
Most common form in darker pigmented
Common in elderly
89
Most common site of acral lentiginous melanoma
Sole, then palm, then subungual
90
Does hx of trauma exclude dx of acral lentiginous melanoma
No
91
Hutchinson's sign
Pigment on nail fold
| Seen in acral lentiginous melanoma
92
Features of sebborrheic keratosis
Well-demarcated, 'stuck-on' appearance*
| Usually, rough surface
93
Breslow thickness
Predicts melanoma survival
| Top of granular layer of the epidermis yo the greatest depth of the tumour in mm
94
Should a bx be done for melanomas
No
95
Diagnostic methods of skin cancer
Hx
Physical examination
Dermascopy
Histopathology
96
Dermoscopy
Simple non-invasive technique to dx skin cancer
Looks at pigment network
Improves sensitivity and specificity for clinical dx
97
Histopathology for making a dx of skin cancer
Gold standard for diagnosing pigmented skin lesion
Based on architectural and cytologic features
Immunohistochemistry may be useful in melanoma dx
98
Sentinel lymph node bx
Staging and prognostic tool for skin cancers
Detects micrometastases in regional LNs
Blue dye + technetium-99 labelled radio colloid solution are injected intradermally at the primary site
99
When should cutaneous lymphoma be considered
```
In eczema which hasn't respond to topical steroids
Usually, scaly red rash
Less itchy than eczema
Not as thick as psoriasis
Slowly progressive over decades
```
100
Features of dermis
Supportive connective tissue matrix
Loss of collagen and elastic
Highly vascularised
101
What is the s/c layer of skin made up of
Loose connective tissue & adipose tissue
102
What is a wound
Loss of integrity of skin tissue
103
What its considered a c/c wound
Disruption in normal healing process (systemic/ local factors)
Slowed/ incomplete healing (usually at infl of proliferative phases)
104
Stages of wound healing
Haemostasis
Infl phase
Proliferative phase
Maturation & remodelling phase
These phases may overlap
105
How long does the infl phase of wound healing last
0-3 days
106
Clinical signs seen in infl stage of wound healing
Rubor
Calor
Tumour
Dolor
107
Haemostasis in wound healing
Aggregation and degranulation of platelets
| Blood clotting and formation of a fibrin plug (eschar) initially fills wound
108
Role of immune cells in infl opals of wound healing
Polymorphonuclear leukocytes, monocytes, macrophages and lymphocytes invade fibrin plug space and secrete growth factors and cytokines to help modulate response
109
Role of fibroblasts in infl phase of wound healing
Help blood vessels from deep fascia and surrounding dermis lay down temp matrix of granulation tissue ---> serve as guide for migrating and proliferating cells
110
How long does the proliferative phase in wound healing last
3-21 days
111
Clinical signs of proliferative phase of wound healing stage
No infl signs
Reduced swelling
Reduced wound size (contraction)
Itch
112
Features of proliferative phase of wound healing
Net collagen synthesis
Increased wound tensile strength
Scar formation
113
Net collagen synthesis in proliferative phase of wound healing
Mediated by growth factors, ECM molecule and their receptors
Extensive cell-cell interactions to control cellular behaviour
114
Increased wound tensile strength in proliferative phase of wound healing
Epidermal cells proliferative and move to wound edge to granulation tissue - closes wound
Wound contcraction via forces within myofibroblast
115
Scar formation in proliferative phase of wound healing
Apoptosis of immune cells, fibroblasts, endothelial cells
| Remaining fibroblasts continue to lay down collagen (I and III)
116
How long does the maturation & remodelling phase last in wound healing
21 days to 2 years
117
Why is the duration of maturation & remodelling phase variable in wound healing
```
Depends on:
Age
Wound type
Body location
Duration of infl phase
```
118
What occurs in the maturation and remodelling phase
Reorganisation of collagen - Type 3 replaced by Tye 1
| Temsile strength improves
119
What can affect speed of wound healing?
```
Size of wound
Blood supply to area
Presence of origin bodies or micro-organisms
Age and health of pt
Nutritional status
Drugs
```
120
Types of wound healing
Primary intention
Secondary intention
Tertiary intention
121
Primary intention e.g. surgical incision
Immediate closure of wound edges when no loss of tissue has occurred
122
Features of primary intention wound healing
Rapid epithelial cover,
Fast healing
Better cosmetic
123
Secondary intention of wound healing
Examples incl excessive trauma, difficult wound closure, tissue loss
Spontaneous healing of wound direct closure (intentionally left open)
124
Tertiary intention of wound healing
Examples incl traumatic injury, dirty surgery, delayed primary intervention or surgical wounds
Initially left open after removal of non-viable tissue
Wound edges brought together after few dats when wound is clean
125
Examples of -pre-cancerous lesions
AK
Dysplastic naevus/ atypical naevus
Bowens disease
Lentigo maligns
126
Examples of benign skin lesions
```
Keratoacanthoma
Seborrheic wart
Cutaneous horn
Viral wart
Epidermoid cyst
```
127
Cryotherapy
Sin lesions frozen w/ cryogen - usually liquid N
128
How does cryotherapy cause cells etch
Ice crystal formation
Osmotic differences --> cell disruption
Iscahemic damage
129
Admins of cryotherapy
~1-2 cm from skin on centre of area
| Form a circular icefield
130
Indications for cryotherapy
```
AK
Viral warts
Seborrheic warts
Bowens disease e
Superficial BCC
```
131
Contraindications of cryotherapy
Pigmented lesion
Malignant lesion
Cold urticaria
132
Efudix (5-Flurouracil)
Antimetabollte cream inhibiting DNA synthesis
133
Admin of efudix cream
OD-BD for 4/52
134
indications of Efudix cream
sBCCs
Multiple AKs
Bowen's disease
135
Indications for imiquimod cream
Warts
sBCCs
AK
Immune response modulator
136
Photodynamic therapy
Activation of topical porphyrin cream to destroy cancer/ pre cancer
Uses red light
137
Indications of photodynamic therapy
AK
Bowen's
sBCC
Multiple or large lesions
138
Admin of curettage and cautery
Inject local anaesthetic
Scrape off lesions
Haemostais by cautery
139
Indications of curettage and cautery
Pyogenic granuloma
Cutaneous horn/ AK
Small nodular BCC
Seborrheic wart
140
Contraindications of curettage and cautery
Pigmented lesions
Most SCCs
Morpheic BCCs
Poor cosmetic reasons e.g. vermillion border, alar rim, nose tip
141
Admin of shave excision
Local anaesthetic
Shave off marked lesion to be removed
Inject w/ blade
Homeostasis by cautery
142
Indications for shave excision
Benign naevi
143
Contraindications for shave excisions
Melanomas
144
How is an excision bx carried out
Mark lesion to be removed
Local anaesthetic
Excise lesion w/ appropriante margin
Side to side closure if possible
145
Indications for excision bx
Suspected tumours
| Pigmented lesions
146
Contraindications for excision bx
INR too high
Pacemaker fitted
Under treatment w/ antiplatelets/anticoag
147
Factors to consider for RT for skin cancers
Type - radiosensitive lesions, morphology of cancer
Site - where surgery may be difficult (e.g. eyelids)
Previous RT
Suitability of other treatments
Pts preferences
148
Moh's surgery - micrographic surgery
Microscopic examination of horizontal section cut from periphery of an excision specimen.
Excellent cure rate but time consuming and expensive
149
Moh's surgery vs other surgeries for skin lesions
Done for recurrent lesions
High risk areas
Aggressive growth
150
Common medico-legal pitfalls w/ removal of skin lesions
Communication about risk and side effects - adequate consents
Size of scars from surgery often bigger than pts expect
Cryotherpya produces a fierce burn like reaction
151
Dx and staging of skin cancer
```
Bx - not from pigmented lesions
Analysis of thickness/ ulceration of excision sample
Sentinel LN bx (SLNB)
CT scans/ MRI
PET scan
```
152
Chemo for skin cancers
Given for metastatic malignant melanoma - usually localised and advanced - isolated limb perfusion, may given dacarbazine
Bleomycin for SCC
153
Targeted therapy for skin cancers looking at BRAF and CKIT
BRAF inhibitors - vermurafenib
| C-KIT - seen in some melanomas, give imatinib
154
Interferon-alpha as adjuvant therapy for skin cancer
Used after removal of melanoma by surgery
| Used to help reduce recurrent of lesion
155
Signs of SCC
Firm, red nodule
Flat sore w/ scanty crust
Fast growing
Irregular border
156
Typical treatments for Aks
Cryo
Topical treatments: 5 fluororacil, disclofenac gel, imiquimod
Curettage and cautery
Photodynamic therapy
157
Signs that an AK is developing into a SCC
Lesions persisting in spite of treatment
Hyperkertaotic lesions
Lesions becoming nodular
158
What does it mean if a cancer is 'in situ'
It is in the epidermis (above basement membrane)
159
What does it mean if a skin cancer is 'invasive'
Cancer is below basement membrane (invaded dermis)
| Increased potential for metastasis due to presence of blood vessels
160
Is seborrheic keratosis benign or malignant
V common benign lesion - no increased risk of malignancy
| Increase in number w/ age
161
When is seborrheic keratosis removed
Cosmetic/ practical reasons
| Can use excision, curettage & cautery, laser, cryosurgery
162
Marjolin ulcer
Invasive SCC formed in site of scar or ulcer
163
Pathogenesis of SCC
Keratinocytes from stratum basale that have replicated and grown up towards surface and down beyond basement membrane
164
SCC on dermatoscope
Central keratinisation or ulceration
| Chaotic vascular pattern
165
Mainstay of SCC treatment
Excision w/ 4-6mm margin
166
Features to look for w/ BCC
```
Rolled pearly border
Telangiectasia
Central ulceration
Bleeding spontaneously
Slow growing
```
167
Features of BCC on dermatoscope
Telangiectasia
Ulceration
Blue/ grey globules
168
Possible evolution of melanoma
```
Bleeding
Itching
Crusting
Oozing
Sensation change
```
169
Melanoma through a dermatoscope
Atypical pigment network
Blue-white veil
Irregular black/ brown globules
170
High risk areas for complications of BCCs
Around the eyes
Nasolabial folds
Around ear canal
Posterior auricular sulcus
171
After examining a suspected melanoma, what additional examinations should be done
Examine remainder of skin - look for more lesions
| Cervical lymph nodes - possible metastasis
172
Definitive treatment of melanoma
Wide surgical excision w/ melanoma
173
Relevant prognostic factors for SCC
Size of the lesion
| Cervical lymph node involvement
174
How can we differentiate hair loss
Diffuse vs patchy
| Scarring or non-scarring
175
Types of excessive hair growth
Hirsutism
| Hypertrichosis
176
Stages of hair growth
Anagen
Catagen
Telogen
177
Anagen phase of hair growth
Long growing phase
178
Catagen phase of hair growth
Short regressing phase
179
Telogen phase of hair growth
Resting/ shedding phase
180
Main types of hair
Languo - fine long hair in foetus
Vellus - fine short hair on all body surfaces
Terminal - coarse long hair
181
Where is terminal hair found
Scalp
Eyebrows
Eyelashes
Pubic areas
182
Structure of nails
Nail is made up of nail plate (hard keratin), which arises from nail matrix at posterior nail fold
Rests on nail bed
183
Examples of nail matrix abnormalities
Nail pitting and ridges
184
Examples of nail bed abnormalities
Splinter haemorrhage
185
Examples of nail plate abnormalities
Discoloured nails
| Thickening of nails
186
What are exclamation mark hairs a pathogonomic sign of
Alopecia areata
187
What is associated w/ an isolated patch of alopecia
Organ-spp autoimmune disease
| Vitiligo
188
Patterns of alopecia areata
Ophiasis
| Patch type
189
Ophiasis
Band of hair loss - usually at circumference of scalp
190
Alopecia areata vs trichotillomania
Regrowth of AA shouldn't have broken hairs, but trichotillomania will
191
Alopecia totalis vs universalis
Totalis - loss of skull hair
| Universalis - loss of all BODY hair
192
Treatment of alopecia areata
```
Consider none
Steroids - top, intralesional, po
Local PUVA
Minoxidil (topical)
Systemic immunosuppression
```
193
Causes of non-scarring hair loss (localised)
Telogen effluvium
Traction alopecia
Skin condns - psoriasis, tinea capitis
194
Trichotillomania
Pt pulls out hair --> broken hair
| Associated w/ psychological disorders in adult pts (OCD spectrum)
195
Features of Telogen effluvium
Diffuse hair shedding following triggering event
No clear demarcation
Hair pull test is +ve
196
Causes of Telogen effluvium
```
Significant infection
Post partum
Stress
Wt loss
Drugs
Excessive sun exposure
Discontinuing OCP
```
197
Examples of drugs causing telogen effluvium
Warfarin
HIgh dose PPIs
MTX
198
What are Beau's line w/ hair shedding pathogonomic for
Telogen Effluvium
199
Causes of non-scarring hair loss (diffuse)
Androgenic - male pattern baldness
Anagen effluvium - chemo
IDA
Trichotillomania
200
Why is it important to differentiate between non-scarring and scarring alopecia
Hair can't grow back in scarring alopecia
| Difference in treatment
201
Ix to perform in scarring alopecia
None
FBC, B12, ferritin
TFTs, fasting glucose, organ-spp antibodies
202
Immunological causes of scarring alopecia
Lichen planopilaris/ frontal bossing
| Lupus
203
Causes of scarring alopecia
```
Immunological
Bacterial/ fungal infection (kerion)
Trauma (burns)/ iatrogenic (RT)
Skin cancers and treatment of
Blistering diseases
```
204
Poor prognostic factors of alopecia areata
Nail signs (pitting or ridging)
Alopecia universalis
Younger age of onset
Hx of atopy
205
Skin condition associated w/ hirsutism
Acne vulgaris
206
Hirsutism
Androgen-dependent pattern of excessive hair growth
207
Common associated condns with hirsutism
Obesity
| PCOS
208
Cases of hirsutism
```
Idiopathic
Postmenopausal
PCOS
Drugs - anabolic steroids
Cushing' syndrome
Neoplastic - ovarian tumours secreting androgens, congenital adrenal hyperplasia
```
209
Ix for hirsutism
Fasting blood glucose
Ovrain ultrasound
Cortisol
Sex hormones
210
Tx of hirsutism
```
Treat underlying cause first
Hair removal (temp) or permanent (laser)
Finasteride
Spiro
COCP e.g. Dianette, Yasmin
```
211
Treatment of androgenic alopecia
Minoxidil topically - up to 6/12 to take effect
Finasteride 1mg od po
Hair transplant
212
Localised causes of hypertrichosis
Naevus-related (e.g. Becker's)
Spina bifida
C/c rubbing
Porphyria cutanea tarda
213
Generalised causes of hypertrichosis
```
Generalised hypertrichosis - X-linked and autosomal dominant
Hypertrichosis languinose
Foetal alcohol syndrome
Paraneoplastic effects
Drugs
Porphyria cutaneous tarda
```
214
Ix for isolated hypertrichosis
```
FBC. U&Es, LFTS, fasting glucose
Serum Fe and ferritin
Hep A-B serology
Serum porphyrins
US liver - refer to gastroenterology if indicated
```
215
Potential causes of nail pitting
```
Psoriasis
Atopic czema
Reiter's disease
Alopecia areata
Pityriasis rosea
Syphilis
```
216
Most likely dx of nail pitting in a younger person associated w/ a rash
Psoriasis
| Atopic eczema
217
Features to help differentiate psoriasis from atopic eczema in the hx
P - uncommonly presents in childhood vs commonly
P - small amount w/ associated sx (arthritis) vs frequently px w/ atopy
P - less strong familial association w/ rash and other sx
P - no allergic triggers
218
Examination features to help differentiate psoriasis from atopic eczema
```
P - sclay appearance vs excoriated
P - extensors affected vs flexures
P - scalp commonly affected vs sometimes
P - behind ears common vs uncommon
P - nail disease more severe
P - plantar involvement common
```
219
Ix for nail pitting
```
Not necessarily needed
Total IgE
Spp RAST
Patch testing if hand or eyelid rash
Skin bx if diagnostic doubt
```
220
Commonest cause of nail pigmentation
Trauma
221
Ddx of pigmented nail streak
```
Physiological (e.g. Africans)
Traumatic
Benign naevus
Addison's
Malignant melanoma
Drugs
```
222
Ways to grade acne
Leed Acne Grading system (1-12)
Mild/ moderate/ severe
Infl/ non-infl
223
Attacking different factors in pathogenesis for acne treatment
Target 1 - microcomedone phase - reduce hyper cornification and follicular occlusion
Target 2 - bacteria & infl
Target 3 - hormonal (+/- topical) - women
224
How do we target microcomedone phase in acne tx
Topical retinoids e.g. isotret, adapalene
Combined w/ top abx --> anti-infl benefits
Top salicylic 2% wash or 20% azalelaic acid wash if intolerant (skin types V esp)
225
Side effects of retinoids
```
Initial flare-up
Teratogenic - must be on 2 forms of contraception
Depression and suicidal ideations
Raised lipids and deranged LFTs
Dry skin, lips, mucosa etc
Skin fragility
```
226
Why might a pt repeat courses of retinoids
Can release months-years later
227
How do we target bacteria and inlet in acne tx
Abx
| Abx w/ BP
228
Topical abx given for acne
Erythromycin and clindamycin
229
Systemic abx given for acne
Lymecycline (OD, not inhibited by food in stomach)
Erythromycin (pregnancy safest)
Minocycline, oxytetracycline, doxycyline, trimethoprim - drug resistance?
230
Main side effect of tetracyclines
Increases sunburn risk
| Cannot be used in pregnancy - yellow teeth in infants
231
How do abx w/ BP work for acne mx
Kills anaerobes by oxygen release in follicular environment
232
How do we target hormones in acne mx
OCP - Dianette (oestrogen and anti-androgen)
| Spiro (anti-androgen)
233
When is is best to use Spiro in acne mx
In older women
| Coeexisting hirsutism or androgenic alopecia
234
Side effects of Spiro for acne mx
Deranges U&E's
Irregular menstrual cycle
Risk of feminising male foetus
235
What constitutes mild acne
Mainly comedomal/ non-infl
236
Open comedones
Blackheads - oxidation of plug in sebaceous filament
| Usually no erythema
237
Closed comedones
Whiteheads
238
Seborrhoea
Oily skin
239
Tx of mild acne
Topical retinoids - adapalene (differin), tretinoin, isotret
Azelaic acid
General advice
If infl - topical BP
240
Tx of moderate acne
Oral treatment +/- topical: abx, hormones
| NB avoid use of different oral and topical abx combin
241
Oral abx for moderate acne
```
Erythromycin - in pregnant, breastfeeding
Tetracyline (1g/day)
Doxy - 100mg/day
Lymecycline - od 408mg/day
Minocycline - 2nd line (costly)
Trimethoprim - 3rd line (400-600mg/ day)
```
Given for 4-6/12
242
Mx of sever acne
Oral isotret (Roaccutane)
243
How does Roaccutane work
Reduces sebum, comedogenesis, P.acnes and anti-infl actions
244
Causes of failure to respond to acne tx
Compliance
P. acne resistance
Gram-ve folliculitis
Incorrect dx
245
NICE Guidelines on referring acne to dermatologist
```
Acne fulminant or gram-ve folliculitis
Severe acne requiring isotret
Dysmorphophobia
Risk fo severe scarring e.g. keloid
Moderate acne unresponsive to 2 courses abx 3/12 long each
Endocrine cause e.g. PCOS
Uncertain dx
```
246
Ddx for acne
Rosacea
Perioral eczema
Milia
Gram-ve follicullitis
247
Acne rosacea as a ddx for acne ddx
```
Occurs in older pts
No nodules, comedones, cysts or scarring
Truncal involvement rare
May see rhinophyma
Associated w/ flushing
```
248
Perioral eczema as a ddx for acne
Pts experience pruirits and dry skin
No comedones
Spares vermillion border
249
Millia as a ddx for acne
May be confused w/ closed comedones
Seen in infraorbital locations
May be seen alongside acne
250
Gram-ve folliculitis as a ddx for acne
Complication of long-term abx therapy for acne
| Hair follicles infected w/ Gram-ve organisms
251
Acne variants
Infantile acne
Acne conglobata
Acne exocoriee
252
Features of infantile acne
Seen in pts <1 year of age
Likely genetic
Not thought to be androgen related
Usually settles within months
253
Features of acne conglobate
Severe nodulocystic acne
Interconnected accesses w. sinuses in between
Scars badly
254
Features of Acne excoriee
Mild/ moderate cane exacerbated by picking (psychological disorder)
Causes secondary infection and scarring - cycle
255
Usual course length of isotret
16/52
256
Why should oral and topical abx not be combined in acne mx
Risk of bacterial resistance
257
What type of contraceptive pill should be avoided in acne mx
Progesterone only
258
Minecycline side effects
Irreversible slate-grey pigmentation of skin
Abnormal LFTs
Induce SLE phenomenon
259
Things to ask in acne hx
Psych effects - what does it stop them from doing, changes they've made
What they advice tried
Products currently in use
Areas - face, back, arms, upper chest
Associated sx
Anythings that makes it worse - cyclical, drugs (steroids)
Fhx
260
Acne nodule
Solid lesion > 5mm raised above skin
| Inflamed and extends to deep layers ---> scarring
261
Acne cyst
Epithelial lined cavity w/ liquid/ semi-solid material
| Heals w/ scarring
262
What is isotret contraindicated in for acne mx
Soya allergies
| Severe peanut allergy
263
What must you test for before commencing isotret for acne
Fasting blood glucose
| Lipids
264
What type of skin cancer does wart virus predispose you to
SCC
265
What types of hereditary factors cause skin cancers
Germ line - e.g. familial melanoma
Acquired mutation e.g. BRAF V600E
Epigenetic - e.g. arsenic toxicity
266
Molecular factors protecting us from skin cancer
```
Constitutional pigmentation
Immune system
DNA repair
Accurate control of cell division
Behaviour - avoiding UVR > covering up > SPF
```
267
Gene mutations seen in BCC
MC1R
PTCH1
PTCH2
RASA1
268
Mutation in Gorlin's syndrome
PTCH2
269
Gorli's syndrome and skin cancer
90% of pts develop multiple BCCs
270
Main symptoms of Gorlin's syndrome
Toothy cysts that develop in teenage years
Bones grow longer and larger
Pits of palms and soles
271
Gene mutations in SCC
MC1R
OCA1/OCA2
XP mutations
RASA1
272
UV damage and diffenrt types of melanoma
Intermittent sunburn - SSMM and nodular
C/c UVR - lentigo MM (and SCC)
UVR-independent - ALM, mucosal and uveal
273
Gene mutations in melanoma
MC1R
BRCA2
P53
BRAF V600E
274
How does vemurafenib treat melanoma
Monoclonal antibody which stops cell from producing BRAF
| BRAF V600E mutation causes too much BRAF --> cells grow and divide
275
What types of melanoma does vemurafenib treat
Metastatic SSMM/ nodular MM
276
What type of melanoma can imatinib treat
Cancers w/ cKIT mutations
| ALM and mucosal melanoma
277
ALM
Acral Lentiginous Melanoma
278
Relationship between skin and psyche
Psychological consequences of skin disease
Skin manifestations of psychiatric disease
Skin condns caused by drug treatment of psychiatric disease
279
Psychological consequences of skin disease
Skin disease have impacts on the person's mental health
| The degree of impact varies depending on many factors (pt and illness related factors)
280
Psychological interventions to help pts w/ skin condns
CBT
Self-help material
Group material
281
Measuring psychosocial stress in skin disease
```
Psoriasis disability index
DLQI
Acne disability questionnaire
Genera health questionnaire (GHQ)
Hamilton scale for anxiety and depression
```
282
How do pts cope w/ and adapt to skin diseases
Adjust to change in appearance
Learning to live w/ uncertainty
Coping w/ reactions from others
Maladpating
283
Features of maladapting to skin disease
Hiding away (long hair, clothing)
Structuring line around disease
Thinking that other (in addn to themselves) are preoccupied with the disease
284
Skin manifestations of psychiatric illness/ psychological distress
```
Deliberate self harm
Dermatitis artefacts
Parasitosis
Dysmorphophobia
Trichotillomania
Excessive handwashing, neurotic excoriations
Signs of alcohol and substance abuse
Sun sensitivity
Nicotine-stained fingers
```
285
Artefactual lesion in skin disease - hypochondriasis
In responses to delusional beliefs
286
Artefactual lesion in skin disease - OCD
Relief of anxiety from repetitive scratching etc
287
Artefactual lesion in skin disease - dermatitis artefacts by proxy
Lesions on another to satisfy psychological need of perpetrators (Munchausen's syndrome by proxy)
288
Epidemiology of dermatitis artefacts
Highest incidence in late teens, early twenties
Often close connection w/ healthcare field
Past hx of serious illness, sexual abuse or loss in childhood not uncommon
289
Clinical picture of D artefacta
Dramatic lesions produced secretly and mysteriously
Not characteristic of known dermatoses
Found in reach of pt's hands
290
Hx and examination of D. artefacta
Complicitly strenuously denied
| 'Hollow hx' - inability to elicit evidence of evolutionary changes
291
Why does the pt cause lesions - DA
Physical expression of emotional problems
Inability to feel cared for unless something being 'done' e..g ointments, ix
'Learnt' such behaviour is rewarding
They have a goal
292
Pts goal in DA
To satisfy an (unconscious) emotional need to be nurtured
293
What is parasitises
Delusion that their bodies are infested w/ some type of organisms
A symptom, not a disease
294
Signs seen in parasitises
'Matchbox' sign - pieces of debris brought as 'proof'
295
What may parasitises be secondary to
Somatic hallucinations
296
Exbom syndrome
Delusional parasitosis
| Treated w/ psychotherapy and antipsychotics
297
Dysmorphobia
Primary complaint of some external physical defect thought to be noticeable yo others, but objectively, appearance lying within normal limits
298
Trichomalacia
Hair roots undergo pathological change in trichotillomania
299
Skin conditions caused by drug treatments of psychiatric disease
Lithium, anticonvulsants (acne-like rash)
Chlorpromazine (photosensitivity)
Steroids
Lamotrigiine
300
What constitutes as a legal inability to use and weigh up information ("process")
Compulsive disorder or phobia may erode capacity
| Temp factors such as shock, fatigue, pain, drugs
301
What is an Advance Decision
A statement of a pt's wish to refuse a particular type of medical treatment or care of they become unable to make/ communicate decisions for themselves
302
What is an Advance Decision limited to
Nothing
Does not have to be just life sustaining treatment
But demands FOR treatment not legally binding
303
When can a pt make an AD
Section 24-26 MCA 2005
| Can apply to physical and mental health
304
When can an AD be overruled
If the pt is sectioned hunted the MHA
305
What needs to be included in an AD
Precisely that tx is to be refused
Circumstances when refusal should apply
Pts can use medical or everyday lang
Details of 3rd party present during discussion
306
Who needs to be informed after a pt has made a AD
Local hospitals just incase pt is admitted unwell
307
What counts as life sustaining tx
To which Dr providing care regards as necessary to sustain life
308
An AD must be
In writing (someone else can write the AD on their behalf)
Signed
Witnessed
Incl a statemnet that the AD decision is to apply even iff life is at risk
309
Limitation of an AD
Cannot refuse action to keep pt comfortable
Connat stop staff offering food and drink
Cannot use it to request euthanasia
Some people go to extreme lengths to make their wishes known
310
How do you decide if AD is valid looking at MCA
Has pt withdrawn the decision?
Has pt made an LPA since then?
Has pt acted inconsistently w/ AD?
Does AD apply to current circumstances and situation?
311
What should be considered when looking at AD validity
How long ago decision was mad e
Change sin personal life
Developments in medical tx
Speaking to family/ friends
312
Wha=y are DNAR order necessary
Resus is commenced without delay - no time for preliminary discussion
Amount to intervention that may be outcome defining
313
Who can make DNAR orders
Most senior clinician in charge of the pt's care
314
What type of skin cancer should be suspected if a central, keratinised plug is seen
SCC
315
Natural hx of SCC
Fungated wound
316
Complications of cryo
```
Hypertrophy scarring
Post-infl pigmentary changes
Nerve damage
Pain
Blistering
Recurrent carcinoma
```
317
Treatment of metastatic non-melanoma skin cancer
Aggressive local surgery, LN dissection and post-op RT and chemo
318
When is radiation therapy a primary option for treating skin cancer
If surgery contraindicated in BCC or SCC
| Pts over 60 are preferred candidates
319
Disadvantages of RT
Lack of margin control
Poor cosmoses in some pts
Prolonged course of therapy
Increased risk for reoccurnace
319
Disadvantages of RT
```
Lack of margin control
Poor cosmoses in some pts
Prolonged course of therapy
Increased risk for reoccurrence
Poor healing on lower leg
Cartilage damage on ear
```
320
Mx of rosacea
```
Identify triggers
Sunscreen
Lymecycline
Topical metronidazole
Topical azelaic acid
Laser
```
321
What is the significance of Breslow’s thickness being > 1mm
Sentinel LN bx is indicated to look for evidence of mets
