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Phase 3 > Dermatology > Flashcards

Dermatology Flashcards

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
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2
Q

What are the layers of the skin?

A

Epidermis
Dermis
Subcutaneous

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3
Q

List the layers of the epidermis from superficial to deep.

A

Stratum corneum
Stratum granulosum
Stratum spinosum
Stratum basale

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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
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5
Q

What is the impact of UV radiation to the skin related to skin cancers?

A

p53 TGS mutated by DNA damage

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6
Q

Describe the effects of chronic UV exposure.

A

loss of skin elasticity, fragility, abnormal pigmentation, haemorrhage of blood vessels, wrinkles, premature ageing

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7
Q

Discuss the 4 skin sensation receptors.

A
  1. Merkel cells - base of epidermis, sustained gentle and localised pressure, assess shape/edge
  2. Meissner corpuscles - immediately below epidermis, sensitive to light touch
  3. Ruffini’s corpuscles - dermis, deep pressure and stretching
  4. Pacinian corpuscles - deep dermis, deep touch, position/proprioception
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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
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9
Q

Name some clinical features of acne.

A
  • papules
  • pustules
  • erythema
  • comedones
  • nodules
  • cysts
  • scarring
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10
Q

Discuss the treatment options for acne including their side effects.

A
  1. Reduce plugging - topical retinoid/benzoyl peroxide. SE = irritant, burning, peeling, bleaching
  2. Reduce bacteria - topical or oral antibiotics. SE = gastro upset
  3. Reduce sebum production - antiandrogen e.g. OCP. SE = possible DVT risk
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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
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12
Q

What is dermatitis?

A

inflammation of the skin

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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

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14
Q

List some endogenous types of dermatitis.

A

atopic, seborrhoeic, discoid, varicose, pompholyx

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15
Q

List some exogenous types of dermatitis.

A

contact (allergic, irritant)

photoreaction (allergic, drug)

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16
Q

What is atopic eczema?

A

itchy inflammatory skin condition associated with asthma, allergic rhinitis, conjunctivitis, hayfever

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17
Q

Which antibody is raised in atopic eczema?

A

IgE

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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
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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
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20
Q

How is contact dermatitis precipitated?

A

irritant - direct noxious effect on skin barrier

allergic - type 4 hypersensitivity reaction

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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
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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

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23
Q

Overgrowth of which organism causes seborrhoeic dermatitis?

A

Pitryosporum Ovale yeast

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24
Q

Which inflammatory skin disease is often an identifier for HIV?

A

seborrheoic dermatitis

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25
Q

What is used in the management of seborrhoeic dermatitis?

A

medicated anti-yeast shampoo, topical antimicrobial and mild steroid, moisturiser

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26
Q

What causes venous dermatitis?

A

incompetence of deep perforating veins causing increased hydrostatic pressure

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27
Q

Which area of the body is most commonly affected by venous dermatitis?

A

lower legs

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28
Q

Discuss the management of venous dermatitis?

A

emollients
topical steroid
compresison bandaging
consider early venous surgical intervention

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29
Q

Define psoriasis.

A

a chronic relapsing and remitting scaling skin disease which may appear at any age and affect any part of the skin

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30
Q

When does psoriasis often peak?

A

two peaks

  • 20-30 y/o
  • 50-60 y/o
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31
Q

Briefly describe the aetiology of psoriasis in three points.

A

T cell mediated autoimmune disease
Abnormal infiltration of T cells - inflammatory cytokines and keratinocyte proliferation
Environmental and genetic factors

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32
Q

List some conditions linked to psoriasis.

A
  • psoriatic arthritis
  • metabolic syndrome
  • liver disease/alcohol misuse
  • depression
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33
Q

PSORS genes e.g. PSORS1 are associated with which disease?

A

psoriasis

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34
Q

What are the different types of psoriasis?

A
  • plaque
  • guttate
  • pustular
  • erythrodermic
  • flexural/inverse
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35
Q

What is the Koebner phenomenon?

A

psoriasis at sites of trauma/scars

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36
Q

Describe the appearance of plaque psoriasis.

A
  • raised areas of inflamed skin covered with silvery-white scaly skin
  • demarcation
  • underlying skin is salmon-pink
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37
Q

Which type of psoriasis appears as ‘teardrop spots’?

A

guttate

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38
Q

In which group of people does palmar/plantar psoriasis occur?

A

smokers

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39
Q

Discuss the treatment of psoriasis.

A
  • topical creams and ointments
  • phototherapy light treatment
  • acitretin
  • methotrexate
  • ciclosporin
  • biological therapies
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40
Q

Which topical therapies are used in the treatment of psoriasis?

A
  • moisturisers
  • steroids
  • agents which slow down keratinocyte proliferation e.g. vit D analogues
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41
Q

Discuss the role of UV phototherapy in the treatment of psoriasis.

A
  • non-specific immunosuppressant therapy
  • can reduce T cell proliferations
  • encourages vit D and reduces skin turnover
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42
Q

What are the short and long term risks of UV phototherapy?

A 
short = burning
long = skin cancer
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43
Q

Describe two pathways which interact to cause skin cancer.

A
  1. Direct action of UV on keratinocytes for neoplastic transformation via DNA damage
  2. Effects of UV on the host’s immune system
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44
Q

What are the 3 main skin cancer types?

A
  • basal cell carcinoma
  • squamous cell carcinoma
  • malignant melanoma
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45
Q

PTCH gene mutation may predispose to which skin cancer?

A

basal-call carcinoma

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46
Q

Where are the majority of BCC found?

A

head and neck/UV exposed sites

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47
Q

Does BCC metastasise?

A

rarely

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48
Q

What are the four BCC subtypes?

A
  • nodular
  • superficial
  • pigmented
  • morphoeic/sclerotic
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49
Q

Describe the appearance of nodular BCC.

A

> 0.5cm raised lesion - shiny, telangectasia, often ulcerated centrally, rolled edge

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50
Q

Which BCC is characterised by superficial proliferation of neoplastic basal cells?

A

superficial BCC

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51
Q

Why is morphoeic/sclerotic BCC hard to diagnose and manage?

A

it infiltrates underneath skin at a slow rate, can’t visualise the whole tumour

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52
Q

What is the gold standard treatment of BCC?

A

surgical excision with 3-4 mm margin

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53
Q

Where does SCC originate from?

A

keratinocytes

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54
Q

What are the pre-malignant variants of SCC?

A
  • actinic keratoses

- Bowens disease

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55
Q

What is Bowens disease?

A

SCC in situ

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56
Q

What is the main cause of SCC?

A

regular exposure to sunlight or other UV radiation

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57
Q

What is the risk of metastasis from a high-risk SCC?

A

10-30%

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58
Q

What are the high risk sites of SCC?

A

ears and lips

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59
Q

Describe the appearance of SCC?

A
  • crusty and scaly due to keratin involvement
  • slight inflammation
  • no shiny rolled margin
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60
Q

What is the gold standard treatment of SCC?

A

surgical excision 4mm

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61
Q

What is a melanoma?

A

malignant tumour of melanocytes

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62
Q

Melanoma is most commonly found in the skin. Name two other sites where they can be found?

A

bowel and eye

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63
Q

Describe the growth pattern of melanoma.

A

radial growth phase, then vertical growth

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64
Q

How is melanoma spread?

A

via lymphatics

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65
Q

List some risk factors for developing melanoma.

A
  • genetic markers
  • UV radiation
  • intermittent burning in unacclimatised fair skin
  • immunosuppression
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66
Q

Discuss staging of melanomas in regards to Breslow depth.

A

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
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67
Q

What are the medical treatment options for melanoma?

A
  • surgical excision (1-2 cm margin)
  • ipilimumab
  • MEK inhibitors
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68
Q

Discuss the long term non-medical management of melanoma.

A
  • imaging/scanning
  • long term follow-up for 5 years
  • assessment for lymph node/organ spread
  • genetic testing in families
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69
Q

What is Gorlin’s syndrome?

A
  • multiple BCC
  • jaw cysts
  • risk of breast cancer
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70
Q

What is Brook Spiegler syndrome?

A
  • multiple BCC

- trichoepitheliomas

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71
Q

What is Gardner syndrome?

A
  • soft tissue tumours
  • polyps
  • bowel cancer
72
Q

What is Cowden’s syndrome?

A
  • multiple hamartomas

- thyroid and breast cancer

73
Q

What bacteria are commonly found as part of the natural skin flora?

A
  • coagulase -ve staph.
  • corynebacterium sp.
  • staph. aureus
  • strep. pyogenes
74
Q

What is impetigo?

A

golden encrusted skin lesions with inflammation localised to the dermis

75
Q

Which bacterial organism caused impetigo?

76
Q

How is impetigo treated?

A
  • usually mild and self-limiting

- treat with topical fusidic acid or systemic antibiotics if required

77
Q

Define tinea.

A

superficial fungal infection of the skin or nails

78
Q

What are the common causes of tinea?

A
  • microsporum
  • epidermophyton
  • trichophyton
79
Q

Discuss the treatment of tinea.

A
  • non-severe: topical therapy - terbinafine cream

- severe/hair/nails: systemic therapy - terbinafine or itraconazole

80
Q

What is a soft tissue abscess?

A

infection within the dermis or fat layers with development of walled off infection and pooled pus

81
Q

Define cellulitis.

A

infection involving dermis

82
Q

Describe the distribution of cellulitis.

A
  • commonly begins on lower limbs

- often tracks through lymphatic system and may involve localised lymph nodes

83
Q

What are the common causes of cellulitis?

A
  • B-haemolytic strep. (group A most common)

- S. aureus

84
Q

Discuss the classification of cellulitis in regards to Enron classification.

A
  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
Q

What is the treatment of a patient with Enron Class 1 cellultis?

A
  • 1st line: oral flucloxacillin
  • 2nd line: oral doxycycline
  • 7 days
86
Q

What is the treatment of a patient with Enron Class 2 cellulitis?

A
  • initial IV flucoxacillin
  • 2nd line vancomycin
  • switch to oral after 48-72 hours
87
Q

What is the treatment of a patient with Enron Class 3/4 cellulitis?

A
  • hospital admission for IV therapy and consideration of surgical management
88
Q

Name some complications of severe cellulitis.

A

local - severe tissue destruction

distant - septic shock

89
Q

What causes streptococcal toxic shock?

A

toxin-producing Group A streptococcus

90
Q

Where is the primary infection of strep. toxic shock typically found?

A

throat or skin/soft tissue

91
Q

How do patients present with toxic shock?

A 
localised infection (not necessarily severe), fever and shock
often have diffuse, faint rash over body/limbs
92
Q

Describe the treatment of strep. toxic shock.

A
  • surgery - drain abscesses
  • antibiotics - penicillin may be ineffective, add clindamycin to reduce toxin production
  • consider pooled human Ig in severe cases
93
Q

What is necrotising fasciitis?

A

immediately life-threatening soft tissue infection with deep tissue involvement

94
Q

Why must you not delay consulting a surgeon if necrotising fasciitis is suspected?

A
  • surgical emergency

- rapidly progressive with extensive tissue damage

95
Q

List the signs and symptoms of necrotising fasciitis.

A
  • rapidly progressive
  • pain out of proportion to clinical signs
  • severe systemic upset
  • presence of visible necrotic tissue
96
Q

What are some differences between type 1 and type 2 necrotising fasciitis?

A
  • 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
Q

Discuss the treatment of necrotising fasciitis.

A
  • requires broad spectrum antibiotic therapy - flux, benpen, gent, clinda, metronidazole
98
Q

Describe the altered microbiology of bite injuries.

A
  • staph and strep still common
  • anaerobes also common
  • pasteurella and capnocytophagia from mammal bites
99
Q

Which antibiotics are commonly used in bite injuries?

A

1st line: co-amoxiclav

2nd line: doxycycline and metronidazole

100
Q

When is prophylactic treatment indicated following bite injury?

A
  • high risk injuries
  • tetanus prophylaxis
  • rabies - bat scratches/bites only in UK
101
Q

Which organism is most common in soft tissue infection in people who inject drugs?

A

staph. aureus

102
Q

What are the implications of high rates of bacteraemia and disseminated infection in people who inject drugs?

A
  • S. aureus bacteraemia
  • DVT
  • multiple pulmonary abscesses
103
Q

What is PVL staphylococcus associated with?

A

recurrent soft tissue boils and abscessed, often over months or even years

104
Q

What steps should you follow if PVL staphylococcus is suspected?

A

obtain cultures and ask lab to do PVL genotyping

105
Q

How is PVL staphylococcus treated?

A
  • treatment with surgical treatment of abscesses
  • antibiotics according to sensitivities e.g. clindamycin to reduce toxin production
  • decolonisation therapy to reduce transmission
106
Q

Differentiate the two types of Herpes Simplex.

A 
1 = stomatitis 'cold sore'
2 = genital herpes
107
Q

How is herpes simplex diagnosed?

A

clinically
blood or vesicle fluid for PCR
serology sometimes helpful

108
Q

Acyclovir is used to treat which viral skin infection?

A

herpes simplex

109
Q

If shingles is diagnosed, which other test should be considered?

A

HIV testing

110
Q

What are the three areas of a burn?

A

zone of coagulation, stasis and hyperaema

111
Q

What is an important complication of paediatric thermal injuries?

112
Q

Group A Strep and Staph. still commonly cause infection in burn wounds but which organisms can opportunistically infect?

A
  • enterococcus
  • pseudomonas
  • bacillus
113
Q

How do you treat burn wound infections?

A
  • debridement of dead or severely infected tissue
  • topical antiseptics
  • systemic antibiotics
114
Q

List four endocrine causes of skin changes.

A

thyroid, diabetes, Cushings/steroid excess, sex hormones

115
Q

Which thyroid abnormality leads to dry skin?

A

hypothyroidism

116
Q

Name two clinical skin manifestations of Grave’s disease.

A 
pretibial myxoderma
thyroid acropachy (finger clubbing)
117
Q

What are some of the skin manifestations of diabetes?

A

leg ulcers, necrobiosis lipoidica, diabetic dermopathy, scleredema, granuloma annulare

118
Q

Describe the appearance of necrobiosis lipoidica.

A

waxy appearance, usually yellow discolouration, often on shins, occasionally ulcerates and scars

119
Q

What does diabetic dermopathy look like?

A

dull-red papules that progress to well-circumscribed, small, round, atrophic hyperpigmented skin lesions usually on the shins

120
Q

What is scleredema?

A

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
Q

What is granuloma annulare?

A

fairly rare, chronic skin condition which presents as reddish bumps on the skin arranged in a circle or ring

122
Q

What are some of the consequences of steroid excess seen in the skin?

A

acne, striae, erythema, gynaecomastia

123
Q

How does Addisons manifest in the skin?

A

hyperpigmentation

acanthosis nigracans

124
Q

List three ways in which testosterone levels may be increased in the body and how this presents.

A

PCOS, testicular tumours, testosterone drug therapy

acne, hirsutism

125
Q

High progesterone levels manifest as acne and dermatitis. What causes this?

A

CAH, contraceptic treatment

126
Q

Name the three ways that internal malignancy may present in the skin.

A
  • necrolytic migratory erythema
  • erythema gyratum repens
  • acanthosis nigricans
127
Q

Describe the appearance of necrolytic migratory erythema.

A

erythematous, scaly plaques on acral, intertriginous and periorificial areas

128
Q

Islet cell tumour of the pancreas is associated with which skin manifestation?

A

necrolytic migratory erythema

129
Q

Which skin disease appears as reddened concentric bands with whorled woodgrain pattern?

A

erythema gyratum repens

130
Q

Which cancers is erythema gyratum associated with?

A

mainly lung cancer

also breast, cervical, GI

131
Q

What is pruritis and why is it associated with erythema gyratum repens?

A

chronic itchy skin

peripheral eosinophilia

132
Q

What is acanthosis nigricans?

A

smooth, velvet-like, hyperkeratotic plaques in intertriginous areas e.g. groin, axillae, neck

133
Q

Differentiate between the three types of recognised acanthosis nigricans.

A
  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
Q

What is a Sister Mary Joseph nodule?

A

a palpable nodule bulging into the umbilicus as a result of metastasis of a malignant cancer in the pelvis or abdomen

135
Q

Which nutritional deficiencies manifest in the skin?

A

vit B, zinc, vit C

136
Q

Low levels of three types of vitamin B manifest in the skin, what are they?

A
  • b6: dermatitis
  • b12: angular chelitis
  • b3: pellagra
137
Q

Acrodermatitis enteropathica is associated with deficiency of which mineral?

138
Q

Describe the clinical presentation of zinc deficiency.

A

pustules, bullae, scaling

139
Q

Zinc deficiency can be either inherited or acquired condition. Which gene mutation is associated with the inherited type?

A

SLC39A - encodes an intestinal zinc transporter

140
Q

How is zinc deficiency treated?

A

zinc supplementation

141
Q

What name is given to vitamin C deficiency and how does it present?

A
  • scurvy
  • punctate purpura/bruising, spiral curly hairs, patchy hyperpigmentation, dry skin, dry hair, non-healing wounds, inflamed gums
142
Q

List five causes of erythema nodosum.

A
  • strep infection
  • pregnancy/oral contraceptive
  • sarcoidosis
  • drug induced
  • bacterial/viral infection
143
Q

What is erythema nodosum?

A

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
Q

What are three causes of pyoderma gangrenosum?

A
  • IBD
  • RA
  • myeloma
145
Q

What is pyoderma gangrenosum?

A

condition that causes tissue to become necrotic, causing deep ulcers that usually occur on the legs

146
Q

List three systemic causes of hair thinning.

A

iron deficiency, lupus, hypothyroidism

147
Q

Name the autoimmune condition that causes hair loss.

A

alopecia areata

148
Q

What are the seven major groups of acute skin reactions?

A 
1 drug reactions
2 toxic epidermal necrolysis
3 Stevens Johnson syndrome
4 erythema multiforme
5 urticaria
6 vasculitis
7 erythroderma
149
Q

What drugs commonly cause acute drug rashes?

A
  • antibiotics e.g. penicillins, trimethoprim
  • NSAIDs
  • chemotherapeutic agents
  • psychotropic
  • anti-epileptic e.g. lamitrigine, carbamaz
150
Q

What are three triggers for cutaneous vasculitis?

A

infection, drugs, connective tissue disease e.g. RA

151
Q

Following a presentation of vasculitis rash, what investigations should be carried out and why?

A

check for systemic vasculitis i.e. renal BP, urinalysis

152
Q

Name two drugs that are responsible for drug-induced psoriasiform rash.

A

lithium, beta blockers

153
Q

What is a fixed drug rash?

A

same area, same drug e.g. paracetamol

154
Q

Describe the symptoms of Steven Johnson syndrome.

A

blistering in mucosal surfaces e.g. lips, skin, eyes

haemorrhagic crusting in lips, skin peeling

155
Q

What drugs can induce SJS?

A

lamotrigine, carbamazepine, allopurinol, sulfonamide antibiotics, and nevirapine

156
Q

Discuss the progression of symptoms in toxic epidermal necrolysis.

A

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
Q

What is the immediate management is TEN is suspected?

A
  • dermatological emergency
  • stop suspect drug
  • in patient management
  • analgesia
  • fluid balance, SCORTEN severity scale
  • special mattress, sheets, non-adherent dressings
  • infection control/prophylaxis
158
Q

What are the signs and symptoms of staphylococcal scalded skin syndrome?

A
  • fevere
  • redness and lesions
  • skin wrinkles and blisters
  • skin exfoliations
  • raw skin recovers
159
Q

Which viruses are able to cause the self-limiting allergic reaction erythema multiforme?

160
Q

Describe the appearance of erythema multiforme.

A
  • target lesions
  • no or mild prodrome
  • never progresses to TEN
161
Q

List some of the immunobullous skin disorders.

A
  • bullous pemphigoid
  • mucous membrane pemphigoid
  • paraneoplastic pemphigoid
  • pemphigus
  • dermatitis herpetiformis
162
Q

What are the symptoms of bullous pemphigoid?

A
  • itching, redness and blisters

- eye involvement with scarring

163
Q

Define pemphigus.

A

a rare group of blistering autoimmune diseases that affect the skin and mucous membranes

164
Q

Describe the treatment strategy for immunobullous disorders.

A
  • 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
Q

Which skin condition is indicative of coeliac disease?

A

dermaititis herpetiformis

166
Q

What is the management plan for dermatitis herpetiformis?

A
  • topical steroids
  • gluten free diet
  • oral dapsone (antibiotic)
167
Q

What are the clinical features of urticaria?

A
  • HIVES - itchy, wheals
  • lesions last < 24 hours
  • non-scarring
168
Q

Describe both immune-mediated and non-immune-mediated urticaria.

A
  1. type 1 allergic IgE response

2. Direct mast cell degranulation e.g. opiates, antibiotics, contrast media, NSAIDs

169
Q

What treatments are available for urticaria?

A

antihistamines, steroids, immunosuppression, omiluzimab

170
Q

What are some of the causes of acute urticaria?

A
  • unknown
  • viral infections
  • medications - NSAIDs, aspirin
  • food
  • parasitic infections
  • physical stimulants - cold, pressure, solar, cholinerguc, aquagenic
171
Q

What name is given to the inflammatory skin disease with redness and scaling that affects nearly the entire cutaneous surface?

A

erythroderma

172
Q

What conditions cause erythroderma?

A

psoriasis, eczema, drug reaction, cutaneous lymphoma

173
Q

Give examples of scarring and non-scarring hair loss.

A
  • 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
Q

What aetiologies are involved in the development of alopecia areata?

A

immune phenomenon, against hair follicles and follicular melanocytes

175
Q

What are the different treatment options available from alopecia areata?

A
  1. Super potent topical corticosteroid e.g. clobetasol

Others: intralesional corticosteroid injections, high dose oral corticosteroids, allergic contact immunotherapy, JAK2 inhibitors

176
Q

What investigations should be carried out in hair loss?

A
  • dermoscopy
  • skin biopsy
  • associated autoimmune bloods
  • fungal mycology
  • ANA/lupus
  • syphilis serology

Phase 3 (10 decks)

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