Dermatology Flashcards
(176 cards)
1
Q
Discuss the role of the skin.
A
- primary barrier to infection
- physiological - body temperature, fluid balance, vit D synthesis
- sensation of heat, cold, touch and pain
2
Q
What are the layers of the skin?
A
Epidermis
Dermis
Subcutaneous
3
Q
List the layers of the epidermis from superficial to deep.
A
Stratum corneum
Stratum granulosum
Stratum spinosum
Stratum basale
4
Q
Give a brief description of the embryology of skin.
A
- derived from ectoderm
- W5 skin of embryo covered by simple cuboidal epithelium
- W7 single squamous layer and basal layer
- M4 intermediate layer formed
- epidermis invaded by melanoblasts during early foetal period
- hair formed in M3
5
Q
What is the impact of UV radiation to the skin related to skin cancers?
A
p53 TGS mutated by DNA damage
6
Q
Describe the effects of chronic UV exposure.
A
loss of skin elasticity, fragility, abnormal pigmentation, haemorrhage of blood vessels, wrinkles, premature ageing
7
Q
Discuss the 4 skin sensation receptors.
A
- Merkel cells - base of epidermis, sustained gentle and localised pressure, assess shape/edge
- Meissner corpuscles - immediately below epidermis, sensitive to light touch
- Ruffini’s corpuscles - dermis, deep pressure and stretching
- Pacinian corpuscles - deep dermis, deep touch, position/proprioception
8
Q
What is the aetiology of acne?
A
- keratin and thick sebum blockage of sebaceous gland
- androgenic increased sebum production and viscosity
- proprioni bacterium inflammation and scarring
9
Q
Name some clinical features of acne.
A
- papules
- pustules
- erythema
- comedones
- nodules
- cysts
- scarring
10
Q
Discuss the treatment options for acne including their side effects.
A
- Reduce plugging - topical retinoid/benzoyl peroxide. SE = irritant, burning, peeling, bleaching
- Reduce bacteria - topical or oral antibiotics. SE = gastro upset
- Reduce sebum production - antiandrogen e.g. OCP. SE = possible DVT risk
11
Q
Describe the use of oral isotretinoin in the treatment of severe acne vulgaris.
A
- concentrated form of vit A
- reduces sebum, plugging and bacteria
- standard course for 16 weeks, 1mg/kg
- SE = mostly trivial. Serious = deranged LFTs, raised lipids, mood disturbance, tertogenicity
- expensive
12
Q
What is dermatitis?
A
inflammation of the skin
13
Q
Name one gene abnormality that may be considered a primary cause of disordered barrier function.
A
filaggrin (on chromosome 1), proteins which bind to keratin fibres in the epidermal cells
14
Q
List some endogenous types of dermatitis.
A
atopic, seborrhoeic, discoid, varicose, pompholyx
15
Q
List some exogenous types of dermatitis.
A
contact (allergic, irritant)
photoreaction (allergic, drug)
16
Q
What is atopic eczema?
A
itchy inflammatory skin condition associated with asthma, allergic rhinitis, conjunctivitis, hayfever
17
Q
Which antibody is raised in atopic eczema?
A
IgE
18
Q
What are the complications of atopic eczema?
A
- bacterial infection - Staph. aureus
- viral infection - molluscum, viral warts, eczema herpeticum
- tiredness
- growth reduction
- psychological impact
19
Q
Describe the management plan of atopic eczema?
A
- emollients
- topical steroids
- bandages
- sedative antihistamines
- antibiotics/anti-virals
- avoidance of exacerbating factors
- systemic drugs e.g. ciclosporin, methotrexate
- Dupilumab - Il4/13 blocker
20
Q
How is contact dermatitis precipitated?
A
irritant - direct noxious effect on skin barrier
allergic - type 4 hypersensitivity reaction
21
Q
What are some common allergens leading to contact dermatitis
A
- nickel - jewellery, zips, coins
- chromate - cement, tanned leather
- cobalt - pigment
- colophony - glue, plasters, adhesive tape
- fragrance - cosmetics, creams, soaps
22
Q
What is seborrhoeic dermatitis? Which areas of the body does it commonly affect?
A
chronic, scaly inflammatory condition
face, scalp. eyebrows, upper chest
23
Q
Overgrowth of which organism causes seborrhoeic dermatitis?
A
Pitryosporum Ovale yeast
24
Q
Which inflammatory skin disease is often an identifier for HIV?
A
seborrheoic dermatitis
25
What is used in the management of seborrhoeic dermatitis?
medicated anti-yeast shampoo, topical antimicrobial and mild steroid, moisturiser
26
What causes venous dermatitis?
incompetence of deep perforating veins causing increased hydrostatic pressure
27
Which area of the body is most commonly affected by venous dermatitis?
lower legs
28
Discuss the management of venous dermatitis?
emollients
topical steroid
compresison bandaging
consider early venous surgical intervention
29
Define psoriasis.
a chronic relapsing and remitting scaling skin disease which may appear at any age and affect any part of the skin
30
When does psoriasis often peak?
two peaks
- 20-30 y/o
- 50-60 y/o
31
Briefly describe the aetiology of psoriasis in three points.
T cell mediated autoimmune disease
Abnormal infiltration of T cells - inflammatory cytokines and keratinocyte proliferation
Environmental and genetic factors
32
List some conditions linked to psoriasis.
- psoriatic arthritis
- metabolic syndrome
- liver disease/alcohol misuse
- depression
33
PSORS genes e.g. PSORS1 are associated with which disease?
psoriasis
34
What are the different types of psoriasis?
- plaque
- guttate
- pustular
- erythrodermic
- flexural/inverse
35
What is the Koebner phenomenon?
psoriasis at sites of trauma/scars
36
Describe the appearance of plaque psoriasis.
- raised areas of inflamed skin covered with silvery-white scaly skin
- demarcation
- underlying skin is salmon-pink
37
Which type of psoriasis appears as 'teardrop spots'?
guttate
38
In which group of people does palmar/plantar psoriasis occur?
smokers
39
Discuss the treatment of psoriasis.
- topical creams and ointments
- phototherapy light treatment
- acitretin
- methotrexate
- ciclosporin
- biological therapies
40
Which topical therapies are used in the treatment of psoriasis?
- moisturisers
- steroids
- agents which slow down keratinocyte proliferation e.g. vit D analogues
41
Discuss the role of UV phototherapy in the treatment of psoriasis.
- non-specific immunosuppressant therapy
- can reduce T cell proliferations
- encourages vit D and reduces skin turnover
42
What are the short and long term risks of UV phototherapy?
```
short = burning
long = skin cancer
```
43
Describe two pathways which interact to cause skin cancer.
1. Direct action of UV on keratinocytes for neoplastic transformation via DNA damage
2. Effects of UV on the host's immune system
44
What are the 3 main skin cancer types?
- basal cell carcinoma
- squamous cell carcinoma
- malignant melanoma
45
PTCH gene mutation may predispose to which skin cancer?
basal-call carcinoma
46
Where are the majority of BCC found?
head and neck/UV exposed sites
47
Does BCC metastasise?
rarely
48
What are the four BCC subtypes?
- nodular
- superficial
- pigmented
- morphoeic/sclerotic
49
Describe the appearance of nodular BCC.
> 0.5cm raised lesion - shiny, telangectasia, often ulcerated centrally, rolled edge
50
Which BCC is characterised by superficial proliferation of neoplastic basal cells?
superficial BCC
51
Why is morphoeic/sclerotic BCC hard to diagnose and manage?
it infiltrates underneath skin at a slow rate, can't visualise the whole tumour
52
What is the gold standard treatment of BCC?
surgical excision with 3-4 mm margin
53
Where does SCC originate from?
keratinocytes
54
What are the pre-malignant variants of SCC?
- actinic keratoses
| - Bowens disease
55
What is Bowens disease?
SCC in situ
56
What is the main cause of SCC?
regular exposure to sunlight or other UV radiation
57
What is the risk of metastasis from a high-risk SCC?
10-30%
58
What are the high risk sites of SCC?
ears and lips
59
Describe the appearance of SCC?
- crusty and scaly due to keratin involvement
- slight inflammation
- no shiny rolled margin
60
What is the gold standard treatment of SCC?
surgical excision 4mm
61
What is a melanoma?
malignant tumour of melanocytes
62
Melanoma is most commonly found in the skin. Name two other sites where they can be found?
bowel and eye
63
Describe the growth pattern of melanoma.
radial growth phase, then vertical growth
64
How is melanoma spread?
via lymphatics
65
List some risk factors for developing melanoma.
- genetic markers
- UV radiation
- intermittent burning in unacclimatised fair skin
- immunosuppression
66
Discuss staging of melanomas in regards to Breslow depth.
5 year survival in non ulcerated tumours is:
- 97% for 0 to 0.1 mm
- 91% for 1.01 to 2.0 mm
- 79% for 2.01 to 4.0 mm
- 71% for > 4.0 mm
67
What are the medical treatment options for melanoma?
- surgical excision (1-2 cm margin)
- ipilimumab
- MEK inhibitors
68
Discuss the long term non-medical management of melanoma.
- imaging/scanning
- long term follow-up for 5 years
- assessment for lymph node/organ spread
- genetic testing in families
69
What is Gorlin's syndrome?
- multiple BCC
- jaw cysts
- risk of breast cancer
70
What is Brook Spiegler syndrome?
- multiple BCC
| - trichoepitheliomas
71
What is Gardner syndrome?
- soft tissue tumours
- polyps
- bowel cancer
72
What is Cowden's syndrome?
- multiple hamartomas
| - thyroid and breast cancer
73
What bacteria are commonly found as part of the natural skin flora?
- coagulase -ve staph.
- corynebacterium sp.
- staph. aureus
- strep. pyogenes
74
What is impetigo?
golden encrusted skin lesions with inflammation localised to the dermis
75
Which bacterial organism caused impetigo?
S. aureus
76
How is impetigo treated?
- usually mild and self-limiting
| - treat with topical fusidic acid or systemic antibiotics if required
77
Define tinea.
superficial fungal infection of the skin or nails
78
What are the common causes of tinea?
- microsporum
- epidermophyton
- trichophyton
79
Discuss the treatment of tinea.
- non-severe: topical therapy - terbinafine cream
| - severe/hair/nails: systemic therapy - terbinafine or itraconazole
80
What is a soft tissue abscess?
infection within the dermis or fat layers with development of walled off infection and pooled pus
81
Define cellulitis.
infection involving dermis
82
Describe the distribution of cellulitis.
- commonly begins on lower limbs
| - often tracks through lymphatic system and may involve localised lymph nodes
83
What are the common causes of cellulitis?
- B-haemolytic strep. (group A most common)
| - S. aureus
84
Discuss the classification of cellulitis in regards to Enron classification.
1. Patient not systemically unwell and no significant co-morbidities.
2. Patient systemically unwell or has significant co-morbidities which may complicate or delay resolution of infection
3. Patient has significant systemic upset or unstable co-morbidities that will interfere with response to treatment or limb threatening vascular compromise
4. Presence of sepsis or severe, life threatening complications
85
What is the treatment of a patient with Enron Class 1 cellultis?
- 1st line: oral flucloxacillin
- 2nd line: oral doxycycline
- 7 days
86
What is the treatment of a patient with Enron Class 2 cellulitis?
- initial IV flucoxacillin
- 2nd line vancomycin
- switch to oral after 48-72 hours
87
What is the treatment of a patient with Enron Class 3/4 cellulitis?
- hospital admission for IV therapy and consideration of surgical management
88
Name some complications of severe cellulitis.
local - severe tissue destruction
| distant - septic shock
89
What causes streptococcal toxic shock?
toxin-producing Group A streptococcus
90
Where is the primary infection of strep. toxic shock typically found?
throat or skin/soft tissue
91
How do patients present with toxic shock?
```
localised infection (not necessarily severe), fever and shock
often have diffuse, faint rash over body/limbs
```
92
Describe the treatment of strep. toxic shock.
- surgery - drain abscesses
- antibiotics - penicillin may be ineffective, add clindamycin to reduce toxin production
- consider pooled human Ig in severe cases
93
What is necrotising fasciitis?
immediately life-threatening soft tissue infection with deep tissue involvement
94
Why must you not delay consulting a surgeon if necrotising fasciitis is suspected?
- surgical emergency
| - rapidly progressive with extensive tissue damage
95
List the signs and symptoms of necrotising fasciitis.
- rapidly progressive
- pain out of proportion to clinical signs
- severe systemic upset
- presence of visible necrotic tissue
96
What are some differences between type 1 and type 2 necrotising fasciitis?
- type 1 usually complicates existing wounds whereas 2 occurs in previously healthy tissue following a minor injury e.g. scratch/sprain
- 1 = mix of bacteria, 2 = Strep. pyogenes
97
Discuss the treatment of necrotising fasciitis.
- requires broad spectrum antibiotic therapy - flux, benpen, gent, clinda, metronidazole
98
Describe the altered microbiology of bite injuries.
- staph and strep still common
- anaerobes also common
- pasteurella and capnocytophagia from mammal bites
99
Which antibiotics are commonly used in bite injuries?
1st line: co-amoxiclav
| 2nd line: doxycycline and metronidazole
100
When is prophylactic treatment indicated following bite injury?
- high risk injuries
- tetanus prophylaxis
- rabies - bat scratches/bites only in UK
101
Which organism is most common in soft tissue infection in people who inject drugs?
staph. aureus
102
What are the implications of high rates of bacteraemia and disseminated infection in people who inject drugs?
- S. aureus bacteraemia
- DVT
- multiple pulmonary abscesses
103
What is PVL staphylococcus associated with?
recurrent soft tissue boils and abscessed, often over months or even years
104
What steps should you follow if PVL staphylococcus is suspected?
obtain cultures and ask lab to do PVL genotyping
105
How is PVL staphylococcus treated?
- treatment with surgical treatment of abscesses
- antibiotics according to sensitivities e.g. clindamycin to reduce toxin production
- decolonisation therapy to reduce transmission
106
Differentiate the two types of Herpes Simplex.
```
1 = stomatitis 'cold sore'
2 = genital herpes
```
107
How is herpes simplex diagnosed?
clinically
blood or vesicle fluid for PCR
serology sometimes helpful
108
Acyclovir is used to treat which viral skin infection?
herpes simplex
109
If shingles is diagnosed, which other test should be considered?
HIV testing
110
What are the three areas of a burn?
zone of coagulation, stasis and hyperaema
111
What is an important complication of paediatric thermal injuries?
TSS
112
Group A Strep and Staph. still commonly cause infection in burn wounds but which organisms can opportunistically infect?
- enterococcus
- pseudomonas
- bacillus
113
How do you treat burn wound infections?
- debridement of dead or severely infected tissue
- topical antiseptics
- systemic antibiotics
114
List four endocrine causes of skin changes.
thyroid, diabetes, Cushings/steroid excess, sex hormones
115
Which thyroid abnormality leads to dry skin?
hypothyroidism
116
Name two clinical skin manifestations of Grave's disease.
```
pretibial myxoderma
thyroid acropachy (finger clubbing)
```
117
What are some of the skin manifestations of diabetes?
leg ulcers, necrobiosis lipoidica, diabetic dermopathy, scleredema, granuloma annulare
118
Describe the appearance of necrobiosis lipoidica.
waxy appearance, usually yellow discolouration, often on shins, occasionally ulcerates and scars
119
What does diabetic dermopathy look like?
dull-red papules that progress to well-circumscribed, small, round, atrophic hyperpigmented skin lesions usually on the shins
120
What is scleredema?
uncommon progressive thickening and hardening of the skin, usually on the areas of the upper back, neck, shoulders and face. The skin may also change colour to red or orange
121
What is granuloma annulare?
fairly rare, chronic skin condition which presents as reddish bumps on the skin arranged in a circle or ring
122
What are some of the consequences of steroid excess seen in the skin?
acne, striae, erythema, gynaecomastia
123
How does Addisons manifest in the skin?
hyperpigmentation
| acanthosis nigracans
124
List three ways in which testosterone levels may be increased in the body and how this presents.
PCOS, testicular tumours, testosterone drug therapy
acne, hirsutism
125
High progesterone levels manifest as acne and dermatitis. What causes this?
CAH, contraceptic treatment
126
Name the three ways that internal malignancy may present in the skin.
- necrolytic migratory erythema
- erythema gyratum repens
- acanthosis nigricans
127
Describe the appearance of necrolytic migratory erythema.
erythematous, scaly plaques on acral, intertriginous and periorificial areas
128
Islet cell tumour of the pancreas is associated with which skin manifestation?
necrolytic migratory erythema
129
Which skin disease appears as reddened concentric bands with whorled woodgrain pattern?
erythema gyratum repens
130
Which cancers is erythema gyratum associated with?
mainly lung cancer
| also breast, cervical, GI
131
What is pruritis and why is it associated with erythema gyratum repens?
chronic itchy skin
| peripheral eosinophilia
132
What is acanthosis nigricans?
smooth, velvet-like, hyperkeratotic plaques in intertriginous areas e.g. groin, axillae, neck
133
Differentiate between the three types of recognised acanthosis nigricans.
1. Associated with malignancy esp gastric adenocarcinoma, sudden onset, more extensive
2. Familial type, AD, no malignancy, from birth
3. Associated with obesity and insulin resistance, most common
134
What is a Sister Mary Joseph nodule?
a palpable nodule bulging into the umbilicus as a result of metastasis of a malignant cancer in the pelvis or abdomen
135
Which nutritional deficiencies manifest in the skin?
vit B, zinc, vit C
136
Low levels of three types of vitamin B manifest in the skin, what are they?
- b6: dermatitis
- b12: angular chelitis
- b3: pellagra
137
Acrodermatitis enteropathica is associated with deficiency of which mineral?
zinc
138
Describe the clinical presentation of zinc deficiency.
pustules, bullae, scaling
139
Zinc deficiency can be either inherited or acquired condition. Which gene mutation is associated with the inherited type?
SLC39A - encodes an intestinal zinc transporter
140
How is zinc deficiency treated?
zinc supplementation
141
What name is given to vitamin C deficiency and how does it present?
- scurvy
- punctate purpura/bruising, spiral curly hairs, patchy hyperpigmentation, dry skin, dry hair, non-healing wounds, inflamed gums
142
List five causes of erythema nodosum.
- strep infection
- pregnancy/oral contraceptive
- sarcoidosis
- drug induced
- bacterial/viral infection
143
What is erythema nodosum?
an inflammatory condition characterised by inflammation of the fat cells under the skin, resulting in tender red nodules or lumps that are usually seen on both shins
144
What are three causes of pyoderma gangrenosum?
- IBD
- RA
- myeloma
145
What is pyoderma gangrenosum?
condition that causes tissue to become necrotic, causing deep ulcers that usually occur on the legs
146
List three systemic causes of hair thinning.
iron deficiency, lupus, hypothyroidism
147
Name the autoimmune condition that causes hair loss.
alopecia areata
148
What are the seven major groups of acute skin reactions?
```
1 drug reactions
2 toxic epidermal necrolysis
3 Stevens Johnson syndrome
4 erythema multiforme
5 urticaria
6 vasculitis
7 erythroderma
```
149
What drugs commonly cause acute drug rashes?
- antibiotics e.g. penicillins, trimethoprim
- NSAIDs
- chemotherapeutic agents
- psychotropic
- anti-epileptic e.g. lamitrigine, carbamaz
150
What are three triggers for cutaneous vasculitis?
infection, drugs, connective tissue disease e.g. RA
151
Following a presentation of vasculitis rash, what investigations should be carried out and why?
check for systemic vasculitis i.e. renal BP, urinalysis
152
Name two drugs that are responsible for drug-induced psoriasiform rash.
lithium, beta blockers
153
What is a fixed drug rash?
same area, same drug e.g. paracetamol
154
Describe the symptoms of Steven Johnson syndrome.
blistering in mucosal surfaces e.g. lips, skin, eyes
| haemorrhagic crusting in lips, skin peeling
155
What drugs can induce SJS?
lamotrigine, carbamazepine, allopurinol, sulfonamide antibiotics, and nevirapine
156
Discuss the progression of symptoms in toxic epidermal necrolysis.
Early symptoms include fever and flu-like symptoms. A few days later the skin begins to blister and peel forming painful raw areas. Mucous membranes, such as the mouth, are also typically involved. Complications include dehydration, sepsis, pneumonia, and multiple organ failure
157
What is the immediate management is TEN is suspected?
- dermatological emergency
- stop suspect drug
- in patient management
- analgesia
- fluid balance, SCORTEN severity scale
- special mattress, sheets, non-adherent dressings
- infection control/prophylaxis
158
What are the signs and symptoms of staphylococcal scalded skin syndrome?
- fevere
- redness and lesions
- skin wrinkles and blisters
- skin exfoliations
- raw skin recovers
159
Which viruses are able to cause the self-limiting allergic reaction erythema multiforme?
HSV, EBV
160
Describe the appearance of erythema multiforme.
- target lesions
- no or mild prodrome
- never progresses to TEN
161
List some of the immunobullous skin disorders.
- bullous pemphigoid
- mucous membrane pemphigoid
- paraneoplastic pemphigoid
- pemphigus
- dermatitis herpetiformis
162
What are the symptoms of bullous pemphigoid?
- itching, redness and blisters
| - eye involvement with scarring
163
Define pemphigus.
a rare group of blistering autoimmune diseases that affect the skin and mucous membranes
164
Describe the treatment strategy for immunobullous disorders.
- reduce autoimmune reaction - oral steroids
- steroid sparing agents - azathioprine
- burst any blisters
- dressings and infection control
- check for oral/mucosal involvement
- consider screen for underlying malignancy
165
Which skin condition is indicative of coeliac disease?
dermaititis herpetiformis
166
What is the management plan for dermatitis herpetiformis?
- topical steroids
- gluten free diet
- oral dapsone (antibiotic)
167
What are the clinical features of urticaria?
- HIVES - itchy, wheals
- lesions last < 24 hours
- non-scarring
168
Describe both immune-mediated and non-immune-mediated urticaria.
1. type 1 allergic IgE response
| 2. Direct mast cell degranulation e.g. opiates, antibiotics, contrast media, NSAIDs
169
What treatments are available for urticaria?
antihistamines, steroids, immunosuppression, omiluzimab
170
What are some of the causes of acute urticaria?
- unknown
- viral infections
- medications - NSAIDs, aspirin
- food
- parasitic infections
- physical stimulants - cold, pressure, solar, cholinerguc, aquagenic
171
What name is given to the inflammatory skin disease with redness and scaling that affects nearly the entire cutaneous surface?
erythroderma
172
What conditions cause erythroderma?
psoriasis, eczema, drug reaction, cutaneous lymphoma
173
Give examples of scarring and non-scarring hair loss.
- scarring: alopecia areata, telogen efflovium, drug-induced, chemotherapy, androgenic alopecia, anorexia/vitamin deficiency, syphilis
- non-scarring: discoid, cutaneous lupus, folliculitis, fibrosing alopecia, lichen planus, fungal infection
174
What aetiologies are involved in the development of alopecia areata?
immune phenomenon, against hair follicles and follicular melanocytes
175
What are the different treatment options available from alopecia areata?
1. Super potent topical corticosteroid e.g. clobetasol
Others: intralesional corticosteroid injections, high dose oral corticosteroids, allergic contact immunotherapy, JAK2 inhibitors
176
What investigations should be carried out in hair loss?
- dermoscopy
- skin biopsy
- associated autoimmune bloods
- fungal mycology
- ANA/lupus
- syphilis serology
