1
Q
Functions of the skin
A
1) Protection - barrier (physical and immunological)
2) Regulation - body temperature, fluid balance, vit D
3) Sensation - heat, cold, touch, and pain. Network of nerve cells detect and relay changes in the environment
2
Q
What are the layers of the epidermis?
A
- Stratum corneum
- Stratum Lucidum
- Stratum Granulosum
- Stratum Spinosum
- Stratum Basale
• Basement membrane
3
Q
In which layer of the epidermis is filaggrin found?
A
stratum corneum
4
Q
Embryology of the skin
A
Epidermis is derived from the ectoderm
5th week - skin of the embryo is covered by simple cuboidal epithelium
7th week - single squamous layer (periderm), and a basal layer
4th month - an intermediate layer, containing several cell layers, is interposed between the basal cells and the periderm
Early foetal period - the epidermis invaded by melanoblasts, cells of the neural crest origin
Hair- 3rd month as an epidermal proliferation into dermis.
Cells of the epithelial root sheath proliferate to form a sebaceous gland bud.
Sweat glands develop as down growths of epithelial cords into dermis.
5
Q
Where in the skin are Langerhans cells found?
A
basal layer
6
Q
How does skin allergy develop?
A
Skin irritation can be nonallergenic or allergenic
Irritation by nonallergenic and allergenic compounds induces Langerhans cell migration and maturation
Langerhans cells migrate from epidermis to draining lymph nodes
Initial sensitization takes 10-14 days from initial exposure to allergen (nickel, dye, rubber etc.)
This is why there may be no response on initial exposure to an allergen
Once an individual is sensitized to a chemical, allergic contact dermatitis can then develop within hours of repeat exposure
7
Q
Damaging effects of ultraviolet light on skin:
A
1) direct cellular damage
• Photoaging
• DNA damage
• Carcinogenesis
2) alterations in immunologic function.
• P53 TSGs are mutated by DNA damage
• implicated in development of (non-) melanoma skin cancers
8
Q
What are effects of Chronic UV exposure?
A
- loss of skin elasticity
- fragility
- abnormal pigmentation
- haemorrhage of blood vessels - bruising/fragility
- Wrinkles and premature ageing
9
Q
Merkel cells
A
Located at the base of the epidermis
respond to sustained gentle and localised pressure
remember: MerkeL respond to Localised pressure
10
Q
Meissner corpuscles
A
situated immediately below epidermis
particularly well represented on the palmar surfaces of the fingers and lips
especially sensitive to light touch (cotton-wool type sensation)
remember: • MeiSSner respond to Soft (light) touch
11
Q
Ruffini’s corpuscles
A
- situated in the dermis
- sensitive to deep pressure and stretching
remember: RUFFini corpuscles respond to “rough” (deep) pressure
12
Q
Pacinian corpuscles
A
mechanoreceptors present deep in the dermis
sensitive only to deep touch, rapid deformation of skin surface and around joints for position/proprioception
13
Q
Macule
A
- Flat area of the skin that is abnormal
* area of skin discoloration
14
Q
Papule
A
• A circumscribed, elevated, solid lesion
15
Q
Pustule
A
- Papule containing purulent material
* i.e. raised and full of puss
16
Q
Plaque
A
elevated, superficial, solid lesion, greater than 1 cm in diameter
Raised, tends to be big
17
Q
Vesicle
A
- Papule containing serous fluid
* i.e. a tiny blister
18
Q
Bulla
A
A raised, circumscribed lesion greater than 0.5 cm that contains serous fluid.
I.e. a giant blister
19
Q
Erythema
A
superficial reddening of the skin, usually in patches
result of injury or irritation causing dilatation of the blood capillaries
20
Q
Ulceration
A
loss of the epidermis
21
Q
Aetiology of acne
A
Androgens increase sebum production and viscosity
Lining of the hair follicles and sebaceous (oil) glands gets blocked by keratin and sebum build up
This causes narrowing
P. acnes bacteria on the skin thrives on trapped sebum
It invades into the oil glands causing a characteristic spot
22
Q
Diagnosis of acne
A
Diagnosis of acne requires a mixture of all three of:
• Papules
• Pustules
• Erythema
May also have:
• Comedones (black heads/white heads)
Markers of much more severe disease:
• Nodules
• Cysts
• Scarring
23
Q
Distribution of acne
A
- Face – most common area
- Chest
- Back / Shoulders – more common in males
- Occasionally legs, scalp
24
Q
Acne subtypes
A
Acne vulgaris
• Papulopustular
• Nodulocystic
• Comedonal
Steroid induced – more truncal distribution than face
Acne fulminans – dermatological emergency
Acne rosacea – tends to affect adults
Acne Inversus (Hidradenitis suppurativa) - Papules, pustules and cysts on the groin, buttocks and other areas
25
How do you grade the severity of acne?
Leeds grading system, grades 1 to 12
26
Treatment of acne
Reduce plugging
• Topical retinoid
• Topical benzoyl peroxide
Reduce bacteria
• Topical antibiotics (erythromycin, clindamycin)
• Oral antibiotics (tetracyclines, erythromycin)
• Benzoyl peroxide reduces bacterial resistance
Reduce sebum production
• Hormones – anti-androgen i.e. Dianette / OCP
• Changes the viscosity of the oil produced and also leads to less sebum production
27
Oral isotretinoin
Roaccutane
* Oral retinoid for severe acne vulgaris
* Concentrated vitamin A
* Reduces sebum, plugging and bacteria
* Remission of acne in around 80% teenagers
* Standard course for 16 weeks
```
Multiple side effects – most are trivial
• Dry lips
• nose bleeds
• dry skin
• myalgia
```
```
Serious side effects
• Deranged LFTs
• Raised lipids
• Mood disturbance
• Teratogenicity - pregnancy prevention programme
```
28
Keloid scarring
• Overgrown scar tissue
Causes:
• Physical trauma
• Burns
• Hugely exaggerated scars as a result of acne
Cannot be reversed
29
Which two pathways lead to the development of skin cancer?
Direct action of UV on target cells (keratinocytes) for neoplastic transformation via DNA damage
Effects of UV on the host's immune system
30
What is the most common type of skin cancer?
basal cell carcinoma
31
Which gene mutation may predispose to BCC?
PTCH gene mutation may predispose to BCC (pronounced ‘patch gene’)
32
Basal cell carcinoma subtypes
* Nodular
* Superficial
* Pigmented
* Morphoeic
33
Nodular Basal cell carcinoma
* Nodule i.e. raised lesion ( > 0.5cm)
* Rolled shiny margin
* Shiny “pearly”
* Telangectasia (broken blood vessels)
* Often ulcerated centrally
34
Superficial Basal cell carcinoma
* No raised nodular appearance
* Rolled shiny margin
* Broken blood vessels
* Usually doesn’t ulcerate
* Indolent superficial spread
35
Pigmented Basal cell carcinoma
* Rolled shiny margin
* Telangiectasia
* Ulceration
36
Treatment – Basal cell carcinoma
Gold standard – Surgical excision with an adequate margin
3-4mm margin of normal looking skin
37
Squamous Cell Carcinoma
* Originates from keratinocytes
* 2nd commonest skin cancer
Appearance:
• keratin – crusty
• no rolled shiny margin
• inflamed, but no specific blood vessels
• no area of skin ulceration unless very aggressive
38
Pre-malignant variants of Squamous Cell Carcinoma
* actinic keratoses
| * Bowens disease = SSC in situ
39
Treatment – Squamous cell carcinoma
* Gold standard - Surgical excision
* 4-5mm margin due to risk of metastasis
* Curettage and cautery in elderly patients
* Symptomatically debulk the tumour
40
management of Pre-malignant skin lesions
• Topical imiquimod / 5-fluorouracil cream
41
Malignant melanoma
* Malignant tumour of melanocytes
* Most common in skin (but can be bowel/eye)
* Accounts for 75% of deaths from skin cancer
* Often affects young, fit people – hard to diagnose
Depth of tumour penetration into skin at presentation determines prognosis
42
Spread of malignant melanoma
Metastatic spread is via lymphatics, but rarely can spread haematogenously or along the skin
43
Risk factors for development of malignant melanoma
```
family history
UV irradiation
sunburns during childhood
high SE status
intermittent burning in fair unacclimatised skin
skin type I/II
```
44
what determines melanoma prognosis?
Breslow depth score
45
Subungual melanoma
under the nail (nailbed is skin)
46
Acral melanoma
* Affects hands and feet
* Tend to present late
* Poor prognosis
* More common in darker skin types
47
Lentigo maligna
• melanoma in situ lesion on sun-damaged skin
48
Melanoma treatment
Surgical excision:
• (Breslow < 1mm) – 1cm margin
• (Breslow > 1mm) – 2cm margin
If metastatic:
• Chemotherapy
• isolated limb perfusion
49
Biologic therapies for melanoma
* Immunotherapy (ipilimumab)
* Immune checkpoint/MEK inhibitors
* antibodies to BRAF genetic defects (vemurafenib)
50
Name 2 Cutaneous tumour syndromes
Gardner Syndrome – soft tissue tumours, polyps, bowel ca
Cowden’s Syndrome – multiple hamartomas thyroid, breast ca
51
Eczema
= Dermatitis - inflammation of the skin
Inflammation in eczema is primarily due to inherited abnormalities in skin “barrier defect”, causing increased permeability and reduces its antimicrobial function
An inherited abnormality in filaggrin expression is considered a primary cause of disordered barrier function.
The gene for filaggrin is on Chromosome 1
52
what is filaggrin?
Filaggrins are filament-associated proteins which bind to keratin fibres in the epidermal cells.
53
Types of eczema
Endogenous
• Atopic eczema – classical type
• Seborrhoeic eczema
• Varicose eczema
Exogenous (external irritants to the skin)
• Contact (allergic, irritant)
• Photoreaction (allergic, drug)
54
Atopic eczema
* Itchy inflammatory skin condition
* Yellow crusting suggests a secondary bacterial infection
```
Associated with atopic conditions:
• Asthma
• allergic rhinitis
• conjunctivitis
• hay fever
```
* high IgE levels
* Genetic and immune aetiology
* 10% of infants affected
* Remission occurs in majority by 15 years
* 2/3 have a family history of atopy
55
Infant atopic eczema
* Itchy
* occasionally vesicular (small blisters)
* often facial component
* secondary infection (yellow crusting)
* < 50% still have eczema by 18 months
occasionally aggravated by food (i.e. milk, eggs, wheat) unlike in adult eczema
Symmetrical distribution
56
complications of infant atopic eczema
* Growth reduction
* Psychological impact
* Bacterial infection due to broken skin
* Viral infection
57
Management of infant atopic eczema
Emollients – ‘reseal’ the skin with a protective film
Topical steroids – targets the inflammatory component
Bandages, antihistamines (sedative) – to prevent scratching
Antibiotics / antivirals (if prone to HSV/eczema herpeticum)
Education for parents and child – specialised eczema nurses
Avoidance of exacerbating factors
Systemic drugs – immune modifications. Very potent drugs
• Ciclosporin
• Methotrexate
Newer biological agents
• Dupilumab – IL-4/IL-13 blocker
58
Contact dermatitis
Precipitated by an exogenous agent
Two types:
• Irritant - direct noxious effect on skin barrier
• Allergic - Type IV hypersensitivity reaction. Immune system is sensitised and reaction occurs on repeated exposure
59
Common allergens causing contact dermatitis
Nickel - Jewellery, zips, scissors, coins, door handles
Fragrance - Cosmetics, creams, soaps
Chromate - Cement, tanned leather
Cobalt - Pigment
60
Seborrhoeic Dermatitis
* Chronic, scaly inflammatory condition
* Often thought to be “dandruff”
* Face, scalp, and eyebrows
* Overgrowth of Pityrosporum Ovale yeast. Natural commensal organism. Thrives on oily parts of the skin
* Can be worse in teenagers
* Identifying illness for HIV
61
Management of Seborrhoeic Dermatitis
Scalp - medicated anti yeast shampoo
Face - anti-microbial, mild steroid
Simple moisturizer
Often improves with UV/sunlight
62
Venous dermatitis
Underlying venous disease causing incompetence of deep perforating veins
This leads to increased hydrostatic pressure
Skin gradually starts to stretch out, and ultimately this causes inflammation and external dermatitis
Symmetrical
Usually in the area with the most gravitational pressure - affects lower legs
Brown discolouration due to haemosiderin deposition
Can cause areas of superficial ulceration
63
Management of Venous dermatitis
Emollient
Mild/moderate topical steroid to target inflammation
Compression bandaging / stockings – to target the valve issues/gravitational effects
Consider venous surgical intervention
64
Psoriasis
a chronic relapsing and remitting scaling skin disease
may appear at any age and affect any part of the skin
common on the lower back
Age onset often two peaks:
• Early onset 20-30y
• Late onset 50-60y
65
psoriasis pathophysiology
T cell mediated autoimmune disease
Abnormal infiltration of T Cells causes release of inflammatory cytokines
Inflammation causes increased keratinocyte proliferation
This is what causes the skin to become scaly and build up (turnover is too fast)
- Inflammation is what causes the redness
Environmental and genetic factors
66
Koebner phenomenon
formation of psoriatic skin lesions on parts of the body that aren't typically where a person with psoriasis experiences lesions
Can appear at the sites of trauma/scars
67
Auspitz's sign
the appearance of punctate bleeding spots when psoriasis scales are scraped off
68
Plaque psoriasis
Most common type of psoriasis
```
Appearance:
salmon pink
well-demarcated
scaly on top
symmetrical
```
Changes seen in the nails:
Onycholysis - nail end lifts off due to plaques underneath the nail
Nail pitting
Dystrophic nails
psoriatic arthritis
69
Guttate psoriasis
* Teardrop/raindrop shape
* Comes on very quickly, often in unwell patients
* Can be triggered by infection (e.g. streptococcal throat infection)
70
pustular psoriasis
* Very inflammatory
* Acute presentation
* Pustules are not infective, but markers of acute inflammation
71
Treatments for psoriasis
In order of increasing effectiveness (and toxicity)
• Topical therapies - moisturisers, steroids
• Phototherapy light treatment
• Acitretin
• Methotrexate
• Ciclosporin
• Biologic therapies
72
Ultraviolet Phototherapy
Non-specific immunosuppressant therapy to the skin
• Eczema
• Acne
• Seborrhoeic dermatitis
* Can reduce T cell proliferations
* Decreases release of inflammatory cytokines
• Encourages Vitamin D (reduces skin turnover)
UV-B light most commonly used – less damaging
73
List some commensal organisms of the skin
* Coagulase negative staphylococci
* Corynebacterium sp.
In areas of skin with less acidic pH:
• Staphylococcus aureus
• Streptococcus pyogenes
Usually not Gram negative bacteria or anaerobic organisms
NB: Anaerobe P. acnes dwells in sweat and sebacious glands
74
Most common organisms causing bacterial skin infection
* Staphylococcus aureus
| * Group A streptococcus
75
Impetigo
Golden encrusted skin lesions with inflammation localised to the dermis.
Most common in children
Highly contagious and may occur in small outbreaks
Caused by S. aureus; usually mild and self limiting
Can treat with topical fusidic acid or topical mupiricin
Usually not severe enough to require oral or systemic antibiotics
NB: Staphylococcus aureus classically crusts
76
how do bacterial and fungal infections of the skin differ?
bacterial infections cause much more inflammation than fungal infections
• Redder
• Hotter
• Erythematous
Fungal infections tend to be less red and not too painful to touch
77
Tinea
Superficial fungal infection of the skin or nails
Very common, particularly on the feet
Demarcated appearance, but appears to be spreading
78
Diagnosis and treatment of tinea
Diagnosis can be made on skin scrapings
Treatment with topical therapy in non-severe cases involving skin alone: terbinafine cream
Systemic therapy in severe cases and those involving hair/nails:
• Terbinafine or itraconazole
Fungal nail infections may require an extended period of oral antifungal therapy
79
Soft tissue abscess
Infection within the dermis or fat layers with development of walled off infection and pooled pus
Best treatment for abscess is always surgical drainage
because antibiotics cannot penetrate abscesses very well
Antibiotics not usually required if abscess fully drained and no surrounding cellulitis
Same causative organisms as cellulitis
• Staph aureus
• Group A strep
80
Panton valentine toxin
Virulence factor (cytotoxin) carried by some Staphylococcus aureus
Association with recurrent soft tissue boils and abscesses
Transmissible – outbreaks occur in families and others living closely together
81
Cellulitis
Infection involving dermis
Usually caused by β-haemolytic streptococci (Gp A Strep most common) and S. aureus
Most commonly begins on the lower limbs
Often tracks through the lymphatic system and may involve localised lymph nodes
May be associated with systemic upset although bacteraemia is relatively uncommon
82
Classification of cellulitis
Enron Classification:
I. Patient not systemically unwell and no significant co-morbidites (i.e. diabetes)
a) <48h antibiotic therapy
b) failure to respond to >48h antibiotic therapy
II. Patient systemically unwell or has significant co-morbidities which may delay resolution of infection
III. Patient has significant systemic upset or unstable co-morbitidies that will interfere with response to treatment
IV. sepsis or life threatening complications
83
Streptococcal Toxic Shock
Caused by toxin producing Group A Streptococcus
Primary infection is typically within the throat or skin/soft tissue
Patients present with localised infection (not necessarily severe), fever and shock
Exotoxins cause massive immune stimulation and cytokine cascade causes blood vessel dilation --> patients often present with a diffuse, faint rash over body/limbs
84
Necrotising fasciitis
Immediately life threatening soft tissue infection with deep tissue involvement
Rapidly progressive (within hours) with extensive tissue damage requiring extensive surgical debridement
85
Signs/symptoms of necrotising fasciitis
* Rapidly progressive
* Pain out of proportion to clinical signs
* Severe systemic upset
* Presence of visible necrotic tissue
86
Antimicrobial treatment of necrotising fasciitis
* Flucloxacillin
* Benzylpenicillin
* Gentamicin
* Metronidazole
* Clindamycin
Remember: Fight Back GMC
NB: Antibiotics are no substitute for surgical intervention
87
Cellulitis differential diagnosis
* DVT
* Thrombophlebitis
* Lyme disease
88
PWID soft tissue infections
Often present late with neglected soft tissue infection
Staphylococcus aureus predominates but infections often polymicrobial
High rates of bacteraemia and disseminated infection
Triad of:
• S. aureus bacteraemia
• DVT
• multiple pulmonary abscesses
Often have endocarditis
Must offer BBV testing
89
Urticaria (hives)
* Itchy, wheals (hives) - red, raised, itchy bumps
* Lesions last <24 hours
* Non-scarring
Immune-mediated
– type 1 allergic IgE response
Non-immune-mediated
– direct mast cell degranulation
– e.g. opiates, antibiotics, contrast media, NSAIDs
90
Morbilliform rash
measles-like rash (red macular rash)
91
Fixed drug rash
causes a rash in a specific place every time you take a drug
can be caused by paracetamol
92
Which drugs commonly cause angioedema?
ACEi
93
Which drugs commonly cause photo-toxic drug rash?
• Affects areas exposed to UV light
Systemic reaction between absorbed drug that has leaked into the skin and UV light
– Tetracyclines
– Isotretinoin (roaccutane)
– Quinine
– bendroflumethiazide
94
What can cause a Pustular drug rash?
antibiotics
95
Lichenoid rash
* Purply itchy rash
* Looks similar to the rash “Lichen planus”
* Can be drug-induced
* Tends to have a white network pattern on top
96
COMMON EXAM QUESTION
what is a drug trigger for psoriasis?
Lithium, Beta blockers
rash that resembles the plaquelike erythematous lesions of psoriasis (Psoriasis–like)
Well demarcated pink erythema with scale
Sudden onset, no FHx
97
Name two Drug induced Blistering disorders
– Steven Johnson Syndrome
| – Toxic epidermal necrolysis
98
Name two Immunobullous diseases
– Bullous pemphigoid
– Pemphigus
immunobullous conditions are characterised by pathogenic autoantibodies directed at target antigens whose function is either cell-to-cell adhesion within the epidermis or adhesion of stratified squamous epithelium to the dermis
target antigens are components of desmosomes or the functional unit of the basement membrane
screen for underlying malignancy – immunobullous diseases can be associated with malignancy
99
Stevens Johnson Syndrome
* Blistering condition
* Often affects mucosal areas
* Some blistering on skin possible
* Can have haemorrhagic crusting on the lips
NB: If < 10% skin involvement, it is SJS not Toxic epidermal necrolysis
100
Toxic epidermal necrolysis (TEN)
Much more extensive than SJS
Looks like a 3rd degree burn, skin becomes necrotic and essentially falls off
Dermatological emergency
Majority of cases are drug induced
If < 10% skin involvement, it is SJS not TEN
>10% of skin involvement = TEN
Common cause of mortality is secondary sepsis
101
Staphylococcal scalded skin syndrome
Characterised by red blistering skin that looks like a burn or scald
caused by the release of exotoxins from S. aureus
Not very systemically unwell
No mucosal involvement
Generalized redness and some peeling
102
Erythema multiforme
hypersensitivity reaction usually triggered by infections, most commonly HSV
presents with a skin eruption characterised by typical Target lesions
acute and self-limiting
103
which skin condition is characterised by target lesions?
Erythema multiforme
104
Bullous pemphigoid
Autoimmune pruritic skin disease
preferentially affects elderly people
formation of blisters (bullae) at the space between the epidermis and dermis skin layers.
classified as a type II hypersensitivity reaction, with the formation of anti-hemidesmosome antibodies
105
Pemphigus
More severe than bullous pemphigoid
Pemphigus is unique from pemphigoid in that the blistering can involve the mucous membranes as well as skin.
causes blisters that slough off and turn into sores
– Sheared pattern
– Superficial split (pemphigus)
Autoantibodies to various skin components
– i.e. basement membrane proteins in BP
106
Dermatitis herpetiformis
(coeliac disease)
Tiny blisters on elbows, knees and buttocks (extensor surfaces)
Topical steroids to treat autoimmune component
Gluten free diet
Oral dapsone
107
Causes of Acute urticaria
* Unknown
* Viral infections
* Medication
* Foods
* Physical stimulants
108
Erythroderma
* Descriptive term
* erythema with >80-90% involvement
```
Causes:
– Psoriasis
– Eczema
– Drug reaction
– Cutaneous lymphoma (unusual)
– others
```
Treat underlying skin disorder
109
Acute generalized exanthematous pustulosis (AGEP)
also known as pustular drug eruption / toxic pustuloderma
rare skin reaction
related to medication administration in 90% of cases
characterized by sudden skin eruptions (numerous sterile pustules)
appear on average five days after medication is started
110
What kinds of systemic disease can manifest with skin changes?
```
o Endocrine disease
o Internal malignancy
o Nutritional deficiency
o Systemic infection
o Systemic inflammatory disease
```
111
Thyroid dermopathy
= pretibial myxoedema
Seen in Grave’s disease
an infiltrative dermopathy
most commonly seen on the shins (pretibial areas)
characterised by swelling and lumpiness of lower legs.
112
Thyroid acropachy
Seen in Grave’s disease
extreme manifestation of autoimmune thyroid disease.
presents with finger clubbing, swelling of digits and toes, and periosteal reaction of extremity bones.
almost always associated with ophthalmopathy and thyroid dermopathy
113
Necrobiosis lipoidica
Seen in diabetes
waxy appearance
yellow discolouration
often localized to bilateral shins
occasionally ulcerates and scars (“shopping trolley distribution” – the area where a shopping trolley would hit) if chronic or with trauma
114
Diabetic dermopathy
The lesions are asymptomatic
red crusted papules
occur on the shins of patients with diabetes.
115
which skin condition is described as having a "Woody texture" and what disease is it associated with?
Scleredema (NB: not scleroderma)
associated with diabetes
116
Which skin condition may be a marker as a precursor to diabetes?
Granuloma annulare
117
Possible skin manifestations of Cushings syndrome/steroid excess
Acne – disproportionate aggressive acne, particularly on the trunk
Striae
Erythema – generalized redness
Gynaecomastia
Global skin atrophy --> easy bruising
118
Possible skin manifestations of Addison's disease /steroid insufficiency
Hyperpigmentation – distinctive bronze discoloration
o Seen in palmar creases and old scars
o Areas of increased skin markings e.g. over extensor surfaces of knees
Acanthosis nigricans
119
Possible skin manifestations of testosterone excess and conditions/treatments that may cause this.
* Acne
* Hirsutism – male pattern
e.g.
Polycystic Ovarian Syndrome
Testicular tumours
Testosterone drug therapy – e.g. topical androgen gels
120
Possible skin manifestations of progesterone excess and conditions/treatments that may cause this.
* Acne
* Dermatitis
E.g.
o Congenital adrenal hyperplasia
o Contraceptive treatment
121
list 3 Cutaneous Signs of Internal Malignancy
* Necrolytic migratory erythema
* Erythema gyratum repens
* Acanthosis nigricans
122
Which skin condition is strongly associated with glucagonomas?
Necrolytic Migratory Erythema
Red, blistering rash that spreads across the skin. Haphazard, irregular plaques
particularly affects the skin around the mouth and distal extremities
o Erythematous
o scaly plaques on acral (peripheral body parts), intertriginous (where two skin areas may touch or rub together), and periorificial areas
123
Which skin condition presents with a whorled woodgrain pattern? What kind of systemic disease is it associated with?
Erythema Gyratum Repens
Significant disproportionate itch and peripheral eosinophilia
Strong association with solid organ malignancy, especially lung cancer
124
Which skin condition is strongly associated with uterine/ovarian tumours?
Sister Mary Joseph Nodule
originates from the umbilicus
125
Describe the cutaneous features associated with Vitamin B Deficiencies
B6 - pyridoxine
• Dermatitis (disproportionate)
B12 - cobalamin
• Angular chelitis
B3 - niacin
• Pellagra (dementia, dermatitis, diarrhoea)
126
Describe the cutaneous features associated with zinc Deficiency
Acrodermatitis Enteropathica
autosomal recessive
caused by mutations in the gene that encodes a membrane protein that binds zinc
In infants, deficiency can follow breast-feeding, when breast milk contains low levels of zinc
```
In adults, disease can occur with:
o total parenteral nutrition without zinc supplements
o alcoholism
o malabsorption states
o inflammatory bowel disease
o bowel surgery
```
127
Describe the cutaneous features associated with Vitamin C Deficiency
```
Scurvy
• Punctate purpura / bruising
• “Corkscrew” spiral curly hairs
• Patchy hyperpimentation
• Dry skin
• Dry hair
• Non-healing wounds
• Inflamed gums
```
128
Erythema nodosum
inflammatory condition
characterized by inflammation of the fat cells under the skin, resulting in tender red nodules or lumps
usually seen on both shins
causes severe pain
```
Underlying causes:
• Streptococcal infection
• Pregnancy
• Sarcoidosis
• Drug induced
• Bacterial / Viral infection
```
129
Pyoderma gangrenosum
condition that causes tissue to become necrotic, causing deep ulcers that usually occur on the legs.
Ulcers usually initially look like small bug bites or papules, and they progress to larger ulcers.
Often affects the shins
• Central area of ulceration with purple rim
• “Overhanging” edge
Associated with:
• Inflammatory Bowel Disease
• Rheumatoid arthritis
• Myeloma
130
Which conditions are associated with pyoderma gangrenosum?
* Inflammatory Bowel Disease
* Rheumatoid arthritis
* Myeloma
131
Which conditions are associated with Generalised hair thinning?
o B12 deficiency
o Iron deficiency
o lupus
o hypothyroidism
132
What kind of conditions cause nail clubbing/nail fold telangectasia?
```
Connective tissue diseases
RA
SLE
scleroderma
dermatomyositis
```
133
differential diagnosis of chronic, red scaly skin
eczema
psoriasis
Seborrheoic dermatitis
134
Urticaria
Condition caused by the abnormal release of histamine within the skin
Not normally the result of allergy
135
Urticaria presentation
characterized by blanching, raised, palpable wheals (hives)
can vary in shape
occur on any skin area; usually transient and migratory.
lesions are often separated by normal skin, but may coalesce rapidly to form large areas of erythematous,
raised lesions that blanch with pressure.
Dermographism may occur (urticarial lesions resulting from light scratching)
136
Urticaria precipitants
```
Heat/cold
pressure
exercise
sunlight
emotional stress
chronic medical conditions (hyperthyroidism, RA, SLE)
```
137
Urticaria treatment
Mainstay – antihistamines. Higher dose than hayfever
```
Cetirizine
Fexofenadine
Loratidine
Chlorpheniramine
Hydroxyzine
```
138
Urticaria - Differential Diagnoses
* Allergic Contact Dermatitis
* Atopic Dermatitis
* Erythema Multiforme
139
Risk factors for leg ulceration
o obesity
o smoking
o hypertension
o history of deep vein thrombosis
140
venous ulcers
usually in gaiter area
caused by sustained venous HTN due to venous insufficiency (e.g. varicose veins, pregnancy, trauma)
RBC pushed out of capillaries due to HTN -> haemosiderin deposition from RBC breakdown
can develop venous eczema due to irritation of the skin by waste products leaking from the blood
Tends to be less painful than arterial, usual more superficial and diffuse with more surrounding skin
changes
141
Arterial ulcers
result of reduced arterial blood flow/tissue perfusion.
Atherosclerosis or peripheral vascular disease is the most common cause
if left untreated, can cause death of tissue
Ulcer development is often rapid with deep destruction of tissue.
limb looks pale and there is a noticeable lack of hair.
Capillary refill is reduced; pedal pulses weak or absent.
classically look punched out and deep
142
What would be the most important initial investigation in a patient with a leg ulcer?
Ankle Brachial Pressure Index ABPI (blood pressure comparison between upper and lower limbs)
should be roughly equal
0.8 ratio might suggest occlusion and need vascular arterial assessment
NB: Compression bandages are used for venous ulcers
If a patient has arterial disease with occlusion, compression bandages will worsen the supply to the
distal limbs, which will cause ischaemic disease
143
What initial treatment would you suggest for a venous leg ulcer?
compression bandages
emollient, topical steroid, avoidance of irritant soaps
Topical steroid
144
Name some other causes for leg ulceration
```
Arterial disease
Connective Tissue Disease ie Lupus
Diabetic
Pressure sores
Skin cancer – eg basal cell ca
Infection, deep fungal
Trauma
Necrobiosis lipoidica
Drug induced
Pyoderma gangrenosum
```
145
How would you confirm a diagnosis of malignant melanoma?
full excision of the whole lesion for diagnostic biopsy and histology
146
Breslow thickness
distance in mm of the furthest tumour cell from the basal layer of the epidermis
prognostic tool for malignant melanoma
147
Prognostic factors in melanoma
Size of presenting lesion
depth of clinical pigmentation (Blue / grey colours)
Anatomical location (e.g. poor prognosis for late presentation acral melanoma e.g. sole foot
Evidence of clinical ulceration
Evidence of resorption e.g. regression
Obvious local metastases / satellites (eg in transit)
148
Assessment of a pigmented lesion
```
A - asymmetry
B - border
C - colour
D - diameter
E - evolution
```
149
treatment options for melanoma
Surgical excision with wide local excision - margin based on Breslow thickness 1cm margin Breslow <1mm
Lymph node dissection if LN involved
Chemotherapeutic agents e.g. BRAF inhibitors
o Vemurafenib
Immunotherapy e.g. nivolumab, ipilimumab
150
Non scarring hair loss - 4 examples
alopecia areata
telogen effluvium (hair cycle disorder)
Drug induced, e.g. Chemotherapy
anorexia / vitamin deficiency
151
scarring hair loss - 4 examples
discoid cutaneous lupus
fibrosing alopecia
lichen planus
fungal infection
152
Localised hair loss causes
alopecia areata
| fungal infection
153
Alopecia Areata
autoimmune disease that causes hair to fall out in round patches
Immune phenomenon against hair follicles and follicular melanocytes (regrowth will be white)
Alopecia Totalis (whole scalp hair loss)
Alopecia Universalis (whole body hair loss)
154
treatment options for the management of alopecia areata
Super potent topical corticosteroid
Intralesional corticosteroid injections
High dose oral corticosteroids (in very rapid onset progressive AA)
Allergic contact immunotherapy
o Induces contact dermatitis
o This makes the immune system distracted from the hair follicle, and allows the hair to grow
biologic agents eg Jak2 Inhibitors
155
Some causes of hair loss
Alopecia Areata
psoriasis
eczema
Fungal infection/ringworm
Syphilis
```
Secondary medical causes
Thyroid disease
systemic lupus
vitamin deficiencies eg iron, B12, zinc
Hormonal
```
156
investigations in hair loss
Dermoscopy
Associated autoimmune bloods
o Thyroid
o Glucose - diabetic
o B12
Fungal mycology
check ANA antibodies
Syphilis serology (multi patch moth eaten hair loss)
Diagnostic skin biopsy including hair follicles
J3
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