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Phase 2a > Dermatology > Flashcards

Dermatology Flashcards

1
Q

What is necrotizing fasciitis?

A

A fulminant, rapidly spreading infection with widespread tissue destruction through all tissues and planes

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2
Q

What is the mortality like for necrotising fasciitis?

A

Very high

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3
Q

What is type 1 necrotizing fasciitis caused by?

A

aerobic and anaerobic bacteria, seen post surgery or in diabetics

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4
Q

What is type 2 necrotizing fasciitis caused by?

A

group A streptococci (GAS), arising spontaneously

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5
Q

What are the symptoms of necrotizing fasciitis?

A

severe pain at site of initial infection with tissue necrosis
spreading infection across all planes
spreading erythema, pain and crepitus
fever, toxicity and pain

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6
Q

What do investigations show in necrotizing fasciitis?

A

increased CRP, ESR, WCC

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7
Q

What is the treatment for necrotizing fasciitis?

A

antibiotics (2 = benzylpenicillin and clindamycin, 1 = broad spectrum), surgical exploration, amputation

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8
Q

What is cellulitis?

A

infection of the deep subcutaneous layer

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9
Q

What are the symptoms of cellulitis?

A

hot and tender area, blisters, low grade fever, lymphedema, poorly demarcated margins

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10
Q

Where about does cellulitis affect and then spread to?

A

Starts in the lower leg and spreads upwards

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11
Q

How does the skin appear in erysipelas?

A

larger area with erythematous and sharply demarcated from normal skin

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12
Q

What causes cellulitis?

A

beta-haemolytic streptococcus, staphylococcus or MRSA

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13
Q

Investigations for cellulitis?

A

swab of toes, antistreptolysin O titre (ASOT) and antiDNAse B titre (ADB)

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14
Q

What is erysipelas?

A

a more superficial infection of cellulitis, often of the face, has a well demarcated edge

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15
Q

What is the treatment of cellulitis?

A

phenoxymethylpenicillin and flucloxacillin (IV or oral depending on how widespread), treat underlying cause, low dose antibiotic prophylaxis if recurrent to prevent further lymphatic damage

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16
Q

What is vasculitis?

A

Inflammatory disorder of blood vessels causing endothelial damage

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17
Q

What are the symptoms of vasculitis?

A

haemorrhagic papules, pustules, nodules, plaques that can erode and ulcerate, don’t blanch from glass slide, fixed livedo reticularis pattern, pyrexia and arthralgia

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18
Q

What is leucocytoclastic vasculitis?

A

the most common cutaneous vasculitis affecting the small vessels

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19
Q

how does leucocytoclastic vasculitis usually appear?

A

on lower legs as a symmetrical palpable purpura

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20
Q

What is the treatment of vasculitis?

A

can resolve spontaneously, analgesia, support stockings, dapsone, prednisolone

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21
Q

What is the cause of leucocytoclastic vasculitis?

A

drugs, infection, inflammatory disease, malignant disease, idopathic

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22
Q

What causes pressure sores?

A

elderly, immobile, unconscious, paralysed from skin ischemia, sustained pressure over bony prominence

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23
Q

What are the four grades of pressure sores?

A

1 - non blanchable erythema of intact skin
2 - partial thickness skin loss of epidermis/dermis
3 - full thickness skin loss involving subcutaneous tissue, not fascia
4 - full thickness skin loss involving muscle, bone, tendons and joint capsule

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24
Q

What is the risk assessment scale called for pressure sores?

A

Norton scale and waterlow pressure sore risk assessment

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25
Q

What is the treatment for pressure sores?

A

bed rest, pillows, air filled cushions, pressure relieving mattress, regular turning, adequate nutrition, non irritant occlusive moist dressings, analgesics, plastic surgery, treat underling cause

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26
Q

What is eczema?

A

superficial skin inflammation with vesicles, redness, oedema, oozing, scaling and pruritis

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27
Q

What is the cause of eczema?

A

Atopy - initial selective activation of Th2 type CD4 lymphocytes in the skin which drive the inflammatory process

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28
Q

How common is eczema and who is most likely to have it?

A 
In 5% of the population
10-20% of children
Genetic disease
More likely if atopic 
20-30% chance of passing onto child
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29
Q

What are some exacerbating factors of eczema?

A

dust mites, food allergies, pets, teething, strong detergents, chemicals, woollen clothes, lack of infection in infancy

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30
Q

What are the clinical features of eczema?

A

itchy erythematous scaly patches in flexures, hyper or hypo pigmented skin, blisters if herpes infection, can be punched out lesions (eczema berpeticum)

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31
Q

Where does eczema commonly occur on the body?

A

elbow, ankles, knees, neck

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32
Q

How does scratching affect eczema?

A

produces exconations, causes skin thickening with exaggerated skin markings, can become infected

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33
Q

What is the treatment of eczema?

A

avoid irritants, emollients to hydrate the skin, topical corticosteroids, mild steroids for face (hydrocortisone) and more potent on body (betamethasone or flucinolone), topical immunomodulators (tacrolimus and pimecrolimus), antibiotics if infected, bandaging, oral prednisolone if severe

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34
Q

What is exogenous eczema?

A

Aka contact dermatitis, acute or chronic skin inflammation with sharply demarcated edges, caused by substances in contact with the skin

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35
Q

What are the causes of exogenous eczema?

A

chemical irritants e.g. industrial and cleaning solvents leads to a sensitisation of T lymphocytes over a period of time

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36
Q

What are the clinical features of exogenous eczema?

A

rash with clear cut demarcation or odd shaped areas of erythema and scaling

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37
Q

How can you test for exogenous eczema?

A

Patch testing with suspected allergen

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38
Q

What is the management of exogenous eczema?

A

remove causative agent, steroid creams for a short period of time, antipruritic for itching relief

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39
Q

What is acne vulgaris?

A

facial rash in adolescents

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40
Q

What causes acne vulgaris?

A

seborrhea (high sebum production - an androgenic hormone), comedo formation with ductal hypercornification, colonisation of the pilosebaceous duct with propionibacterium acnes and inflammation of the pilosenaceous unit

follicular epidermal hyper proliferation, blockage of pilosebaceous units with surrounding inflammation , increased sebum production and infection with Propionibacterium acnes via activation of Toll like receptor 2, leading to inflammatory cytokine production

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41
Q

What are the symptoms of acne vulgaris?

A

open (black) or closed (white) comedones, inflammatory papules, pustules, greasy skin (seborrhoea), rupture of inflamed lesions lead to deep seated dermal inflammation and nodulystic lesions, facial scarring

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42
Q

Where does acne vulgaris commonly occur on the body?

A

face, back and sternal areas

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43
Q

What is infantile acne?

A

facial acne in infants and sometimes cystic

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44
Q

What causes infantile acne?

A

maternal androgen influence

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45
Q

What is steroid acne?

A

Occurs secondary to corticosteroid therapy of Cushings, appearing as pustular folliculitis on trunk

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46
Q

What is oil acne?

A

Seen in industrial workers with prolonged oil contact, common on the legs

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47
Q

What is acne fulminars?

A

severe, necrotic and crusted acne lesions

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48
Q

Who is acne fulminars seen in?

A

Rare and in young male adolescents

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49
Q

What is the treatment of acne fulminars?

A

oral prednisolone, analgesics and oral isotretinoin

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50
Q

What are the symptoms of acne fulminars?

A

malaise, pyrexia, arthralgia, bone pain due to sterile bone cysts

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51
Q

What is acne conglobate?

A

cystic acne with abscesses and interconnecting sinuses

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52
Q

What is acne excoriee?

A

deeply exconated and pickled acne with scarring

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53
Q

Who is most like to acquire acne excoriee?

A

Females

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54
Q

What is follicular occlusion triad?

A

severe nodulocystic acne, dissecting cellulitis of the scalp, hidraderitis suppurativa

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55
Q

What is the cause of follicular occlusion triad?

A

Follicular occlusion

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56
Q

Who is most likely to have follicular occlusion triad?

A

Black Africans, rare

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57
Q

What is the 1st line treatment of acne?

A

topical agents e.g. keratolytics
topical retinoids e.g. tretinoin or retinoid like agents
topical antibiotics e.g. crythromycin for inflammatory acne

benzoyl peroxide and azelaic acid (antimicrobial, comedolytic and keratolytic properties)

retinoids, nicotinamide

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58
Q

What is the 2nd line treatment of acne?

A

low dose oral antibiotics for 3-4 months e.g. oxytetracycline, minocycline, erythromycin
hormonal treatment with cyproteroneacetate or ethinylestradiol

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59
Q

What is a side effect of 2nd line acne treatment?

A

DVT

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60
Q

What is the 3rd line treatment of acne?

A

oral retinoid e.g. isotretinoin
synthetic vitamin A analogue that affects cell growth and differentiation
tetratogenic

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61
Q

What is 3rd line acne treatment contraindicated for and what measures prevent this?

A

pregnancy, so must have test and contraceptive advice before

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62
Q

What is psoriasis?

A

A papulo squamous disorder with well demarcated red scaly plaques and inflamed skin - remission and relapses common

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63
Q

Who is most likely to get psoriasis?

A

male = female
common n 16-22 and 55-60years
2% of pop.

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64
Q

What is the cause of psoriasis?

A

group A streptococcus, lithium, UV light, alcohol and stress

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65
Q

How does psoriasis occur?

A

driven by T lymphocytes , resulting in upregulation of Th1-type T cell cytokines and adhesion molecules

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66
Q

What will a skin biopsy show of psoriasis?

A

epidermal ocanthosis and parakeratosis, increased skin turnover, absent granular layer, hyperproliferation, thickened epidermis

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67
Q

What are the clinical features of chronic plaque psoriasis?

A

pinkish red scaly plaques and silver scale on extensor surfaces or sites of trauma, becomes itchy and sore, is lifelong (arthritis and nail changes can accompany it)

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68
Q

What are the clinical features of flexural psoriasis

A

well demarcated, red glazed plaques confined to flexures

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69
Q

Where does flexural psoriasis commonly appear?

A

at groin, nasal cleft and sub mammary areas

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70
Q

How does guttate psoriasis appear on the skin?

A

explosive eruption of very small circular plaques over the trunk caused by streptococcal infections

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71
Q

When does guttate psoriasis commonly occur?

A

2 weeks after streptococci sore throat

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72
Q

In who does guttate psoriasis normally appear in?

A

children and young adults

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73
Q

How does erythrodermic and pustular psoriasis normally appear?

A

pustular psoriasis on hands and feet

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74
Q

What symptoms usually accompany erythrodermic and pustular psoriasis?

A

malaise, pyrexia, circulatory disturbance (systemically unwell)

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75
Q

What type of nail changes can occur in psoriasis?

A

pitting of the nail plate, distal separation of nail plate, yellow brown discolouration, sublingual hyperkeratosis, damaged nail matrix

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76
Q

What is the treatment of psoriasis?

A

topical treatment, phototherapy, systemic therapy and cytokine modulators

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77
Q

How does topical therapy treat psoriasis?

A

hydrates skin, anti proliferative, vitamin D analgues e.g. calcpotriol and calcitrol reduces cell division, coal tar, tazorotene and corticosteroids, topical dithronol inhibits DNA synthesis but can stain the skin, salicyclic acid acts as a keratolytic and helps scalp

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78
Q

How does phototherapy treat psoriasis?

A

UV A/B radiation in conjunction with a photosensitising agent, good for extensive psoriasis

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79
Q

What are risks of phototherapy treatment in psoriasis?

A

can exaggerate skin aging and increase risk of UV induced skin cancer

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80
Q

How does systemic therapy treat psoriasis?

A

oral retinoic acid derivatives e.g. acitretin or etretinate, immunosuppressives e.g. methotrexate or ciclosporin, biological agents e.g. TNF a blockers can all be used in resistant disease or severe, coal tar therapy, dithranol

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81
Q

What is the risk of retinoic acid derivatives in psoriasis?

A

They are teratogenic so CI if pregnant

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82
Q

What are the most common causes of skin cancer?

A

sun exposure, genetics and ethnicity

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83
Q

What is the most common type of malignant skin tumour?

A

basal cell carcinoma (rodent ulcer)

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84
Q

What is the cause of basal cell carcinoma?

A

excessive sun exposure and Gorlins syndrome, immunosuprresion

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85
Q

Why does Gorlins syndrome cause basal cell carcinoma?

A

mutation in the PTCH1 gene

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86
Q

What is the appearance of a basal cell carcinoma?

A

papule or nodule that can ulcerate, telangiectasia or pearly edge over the tumour, flat diffuse superficial form, ill defined morpreic variant

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87
Q

What is the nature of a basal cell carcinoma?

A

slow growth, can erode structures, rarely metastases

88
Q

What is the treatment of basal cell carcinoma?

A

surgical excision, photodynamic therapy, cryotherapy, imiquimod cream, radiotherapy, Mohs micrographic surgery

89
Q

How common is squamous cell carcinoma?

A

It is the second most common metastatic skin cancer.

90
Q

What is the cause of squamous cell carcinoma?

A

Sun exposure or develop from pre existing skin tumours, immunosuppressed, arsenic ingestion

91
Q

What is the nature of squamous cell carcinoma?

A

very aggressive and can metastasize especially lower lip and ear

92
Q

What is the appearance of squamous cell carcinoma?

A

keratotic, ill defined nodules that can ulcerate

93
Q

What is the treatment of squamous cell carcinoma?

A

surgical excision and radiotherapy

94
Q

What are risk factors for malignant melanoma?

A

pale skin, sun exposure, multiple melanocytic naevii (>50), sun sensitivity, immunosuppression, atypical mole syndrome, giant congenital melanocytic naevi, lentigo maligna, family history

95
Q

What is the most serious skin tumour?

A

Malignant melanoma due to early metastases and death

96
Q

What could be a potential cause of malignant melanoma?

A

mutation in B-RAF and oncogene and tumour suppressor proteins linked

97
Q

What is the appearance does lentigo maligna melanoma?

A

papule, signalling invasive tumour

98
Q

What is the appearance of superficial spreading malignant melanoma?

A

large, flat, irregular pigmented lesion

99
Q

What is the appearance of a nodular malignant melanoma?

A

pigmented nodule that can bleed and ulcerate

100
Q

What is the appearance of acral lentiginous malignant melanoma?

A

pigmented on palm, sole and under nail

101
Q

What is the treatment of malignant melanoma?

A

surgery, sentinel node biopsy, radiotherapy, immunotherapy, chemotherapy, Ipilunnumas, vemurafenis

102
Q

What is the appearance of a melanocytic naevi (mole)?

A

flat, brown macule with proliferation of melanocytes at the dermoepidermal junction which then grows into dermis causing elevation above skin surface, even pigmentation and regular border

103
Q

Who is most likely to get a melanocytic naevi?

A

white skinned people, increased chance with age

104
Q

What can melanocytic naevi mature into?

A

mature into a dermal naevus with a loss of pigment

105
Q

What causes a blue naevus and what is its symptoms?

A

caused melanocyte proliferation deep in mid dermis and is asymptomatic

106
Q

What is the appearance of a basal cell papilloma (seborrhoeic wart)?

A

can be flesh coloured, brown, black or greasy with an irregular surface, look stuck on to skin, have tiny keratin cysts on surface

107
Q

What is the treatment of basal cell papilloma?

A

cryotherapy or curettage

108
Q

What is the appearance of a dermato fibroma (histocytoma)?

A

Firm, elevated pigmented nodule with a peripheral ring of pigmentation, mainly in legs

109
Q

Who is most likely to get a dermato fibroma?

110
Q

What does a dermato fibroma consist of?

A

histocytes, blood vessels, fibrosis

111
Q

What is the treatment of a dermato fibroma?

A

surgical excision

112
Q

What is the appearance of a epidermoid cyst?

A

cystic swelling of skin with central punctum and cheesy keratin

113
Q

What is a complication of an epidermoid cyst?

A

They can rupture and cause dermal inflammation

114
Q

What is the appearance of a pilar cyst (trichilemmal cyst)?

A

smooth cysts without punctum on scalp, can be multiple of familial

115
Q

What is the cause of a keratohcanthoma?

A

sun exposure

116
Q

What is a kerotohcanthoma?

A

a rapidly growing epidermal tumour which can lead to central necrosis and ulceration

117
Q

What is a pyogenic granuloma?

A

a benign overgrowth of blood vessels, readily bleed

118
Q

What is the appearance of a pyogenic granuloma?

A

rapidly growing, pinkish red nodule, on fingers and lips

119
Q

What is the cause of a pyogenic granuloma?

A

follows trauma

120
Q

What is a cherry angioma?

A

a benign angiokeratomas

121
Q

What is the appearance of a cherry angioma?

A

tiny pinpoint red papules, especially on trunk

122
Q

What is the treatment of a cherry angioma?

A

No treatment is needed

123
Q

What is the appearance of a solar keratose (actinic karatose)?

A

erythematous silver scaly papules or patches with a conical surface and a red base

124
Q

What does the surrounding skin of a solar keratose look like?

A

skin is inelastic, wrinkled and shows flat brown macules due to solar damage

125
Q

What maliganant cancer can solar keratose develop into?

A

squamous cell carcinoma

126
Q

What is the treatment of a solar keratose?

A

cryotherapy, topical 5 flurouracil cream, 5%imiquimod cream, diclofenac gel

127
Q

What is Bowens disease?

A

intraepidermal carcinoma in situ that can become invasive, seen on womens legs

128
Q

What are risk factors for Bowens disease?

A

female, sun exposure, age, HPV, immunocompromised, HIV

129
Q

What does Bowens disease neighbouring skin look like?

130
Q

What is the appearance of Bowens disease?

A

can be non specific erythema or warty thickening

131
Q

What is the treatment of Bowens disease?

A

topical 5 flurouracil, 5% imiquimod cream, cryotherapy, curettage, photodynamic therap, tissue destructive layer

132
Q

What is the appearance of atypical mole syndrome?

A

individual lesions with irregular pigmentation and border with large number of melanocytic naevi in childhood

133
Q

What does the histology show in atypical mole syndrome?

A

cytological and architectural atypia

134
Q

What is the treatment of atypical mole syndrome?

A

Regular review and excise suspicions due to risk of developing malignant melanoma

135
Q

What occurs in giant congenital melanocytic naevi?

A

large moles present at birth and large lesions, >20cm

136
Q

What is the treatment of giant congenital melanocytic naevi?

A

Regular review and excise suspicions due to risk of developing malignant melanoma

137
Q

What is the appearance of lentigo maligna?

A

slow growing macular area of pigmentation on face of elderly, irregular pigmentation and border

138
Q

what is the treatment of lentigo maligna?

A

excision or 5% imiquimod cream

139
Q

What is a leg ulcer?

A

a chronic sore on your leg that take more than 4-6 weeks to heal

140
Q

What is the most common type of leg ulcer?

141
Q

Where on the leg does a venous ulcer normally occur?

A

medial aspect , just over the ankle

142
Q

What are the characteristics of a venous leg ulcer?

A

shallow, with flat margins, painful, rred and flaky skin on legs, over bony prominences

143
Q

What are the causes of a venous ulcer?

A

dvt, varicose veins, reduced mobility, traumatic injury, obesity, pregnancy, non healing ulcer, recurrent phlebitis, previous vein surgery - these all cause venous hypertension

144
Q

What preventative factors can be done to prevent leg ulcers?

A

lose weight, compression stocking, execrcise regularly, elevate leg, stop smoking

145
Q

What other conditions are associated with venous ulcers?

A

oedema, venous dermatitis, varicositites, lipodermasclerosis, varicose veins

146
Q

What examinations should be done for leg ulcers?

A

serial measurement of ulcer, assess the type of edge, assess base, note location, smell, surrounding skin, infection, peripheral pulses, sensation, varicose veins, peripheral oedema, BP, BMI, Doppler study, duplex US

147
Q

What is the treatment of an ulcer?

A

preventative measures, antiplatelet therapy, avascular surgery, clean and dress the wound, compression bandages, antibiotics, diuretics for oedema, analgesics, split thickness skingrafing

148
Q

What are the characteristics of an arterial leg ulcer?

A

lateral tibial area on the leg, punched out, occasionally deep, irregular in shape, unhealthy appearance of wound bed, necrotic tissue, low exudate

149
Q

What does the surrounding skin of an arterial leg ulcer look like?

A

thin, shiny, dry sin, no hair, cool o touch, pallor on leg elevation, absent or weak pulses

150
Q

What does the surrounding skin of a venous leg ulcer look like?

A

haemosiderin staining, thickening and fibrosis, dilated veins at ankle, crusty, dry and hyperkaratoic skin, eczema, itchy, oedema

151
Q

What is the pain like in a venous leg ulcer?

A

throbbing, aching, heavy

152
Q

What is the pain like in an arterial leg ulcer?

A

Intermittent claudication, worse at night

153
Q

What are diseases associated with arterial disease?

A

diabetes, hypertension, smoking, vascular disease, obesity, inability to elevate limb

154
Q

In who is a venous leg ulcer most commonly found?

A

In women, and older people

155
Q

Where are neuropathic legs ulcers seen?

A

In pressure points in the foot

156
Q

What is the treatment of a neuropathic leg ulcer?

A

keep foot clean, remove pressure, paediatrist, treat diabetes

157
Q

What is a common disease associated with neuropathic leg ulcers?

158
Q

What is a ankle brachial plexus index used for, give an advantage and disadvantage?

A

assessment of arterial disease, more sensitive than Doppler study, but can be falsely positive in diabetes and atherosclerosis due to calcification

159
Q

What are the 3 layers of the skin?

A

epidermis, dermis and subcutis

160
Q

What structures are in the dermis?

A

hair follicles, sweat glands, blood, lymphatics, vessels and nerves

161
Q

What makes up the epidermis?

A

keratinocytes, melanocytes, Langerhan cells

162
Q

What makes up the dermis?

A

fibroblasts

163
Q

What makes up the subcutis?

164
Q

Functions of the skin?

A

structure, protection, fluid balance, temperature ocntrol, sensation, sun protection, odour

165
Q

Basic topical therapies and their uses?

A

creams (water based) and ointments (oil based)
emollients - moisturise dry skin
corticosteroids - anti inflammatory
calcineurin inhibitors - locally immunosuppressive
antivirals/antibiotics - infection, infected antifungals, eczema, acne
vit d analogues/dithranol/tar for psoriasis

166
Q

Types of skin lesion?

A

macule, papule, nodule, pustule, blister, plaque, ulcer

167
Q

Treatment of child atopic eczema?

A

emollients, then topical steroids then calcineurin inhibitors (adults is the same but then use systemic drugs e.g. azathioprine, ciclosporin, methotrexate)

168
Q

Symptoms of scabies?

A

similar looking to eczema but has BURROWS

169
Q

Symptoms of urticaria?

A

red patches (erythema) and weals (mm or cm, red or white, mintues or hours) in the skin, releasing histamine causing small blood vessels to leak into tissue swelling, itching and burning, swelling of the face

170
Q

Treatment of urticaria?

A

oral antihistamines e.g. loratadine or chlorpheniramine

171
Q

Symptoms of guttate psoriasis?

A

multiple scaly lesions on trunk (previous throat infection)

172
Q

Treatment of guttate psoriasis?

A

topical steroids, vit d analoguem UVB

173
Q

Presentation of pityriasis rosea?

A

in young adults, with single herald patch on trunk, caused by a viral infection

174
Q

DD for a sudden rash?

A

drug eruption, guttate psoriasis, pityriasis rosea, viral exanthem, plaque psoriasis

175
Q

DD of a changing pigment lesion?

A

malignant melanoma (cancerous), melanocytic naevus (benign from sun/pregnancy), seboorroeic wart (elderly)

176
Q

DD of adult with red face?

A

adolescent with acne, adult with rosacea, seborrhoeic dermatitis

177
Q

DD of old person with facial tumour?

A

basal cell carcinoma, squamous cell carcinoma

178
Q

DD of leg ulceration?

A

venous/arterial/neuropathic ulcer, vasculitis

179
Q

DD for hair loss?

A

male pattern (androgenetic type has strong genetic influences), alopecia areata (genetics and autoimmune), scarring apolpecia (causes by SLE, severe infections)

180
Q

Treatment for male pattern hair loss?

A

topical minoxidil, oral finasteride

181
Q

Treatment of alopecia areata?

A

topical or intra lesional steroids

182
Q

What is erysipelas?

A

an infection of streptococcus with sudden onset, erythematous and swollen, unwell and pyrexia, tender skin, treat with antibiotics

183
Q

What is impetigo?

A

infection with staph aureus

184
Q

Causes of old person with generalised pruritus?

A

investigate for kidney, liver, endocrine and blood disease

185
Q

What is hirsutism?

A

growth of terminal hair in a male pattern in a women caused by androgen excess or idiopathic

186
Q

What is hypertrichosis?

A

excess terminal hair growth in a non androgen distribution

187
Q

Treatment of hirsutism?

A

depilating creams, waxing, shaving, electrolysis laser

188
Q

What is seborrhoeic dermatitis?

A

symmetrical cheeks, forehead and scalp, can spread to upper trunk, with scaling and redness, reporting with itching and dandruff with overgrowth of yeasts (pityrosporum) - cradle cap if in infants

189
Q

Treatment of seborrhoeic dematitis?

A

antifungal agent and steroid (not for scalp) e.g. keratolytic treatment

190
Q

How does adult with rosacea present?

A

older person with pustules and erythema but no blackheads, rhinophyma (thickening of skin on nose), leading to flushing, burning and sensitive skin, blepharitis (dry eyes with inflamed eyelid margin), telangectasia (prominent blood vessels)

191
Q

Treatment of adult with rosacea?

A

topical metronidazole and oral tetracycline

azelaic acid, erythromycin, isotretinoin

192
Q

Causes of pigmented skin lesions?

A

mole, seborrhoeic wart, freckle, basal cell carcinoma, angioma

193
Q

Why are pigmented skin lesions so important?

A

99% of melanomas present as a pigmented lesion

194
Q

Risk factors for melanoma?

A

high density freckles, red hair, >100 moles, >5 atypical moles, family history

195
Q

Early signs of melanoma?

A

pigmented skin lesions getting bigger and getting darker, irregular shape and border, bleeding, itching

196
Q

What is the ABCDE of melanoma?

A

asymmetry, border irregulaity, colour variabilty, diamete >5mm, elevation irregularity

197
Q

Type of melanoma?

A

superficial spreading (ssmm), nodular, lentigo maligna (usually face), acral (restricted to palsm and soles)

198
Q

Treatment of melanoma?

A

surgical excision of 1-3cm, B-RAF inhibitors e.g. vemurafenib, immunotherapy with PD-1 inhibitors e.g. nivolumab

199
Q

Prognosis of melanoma?

A

breslow thickness: thin lesions

200
Q

Methods to protect yourself from the sun?

A

spf15, higher if fair, sunblock for lips and nose, sunscreem 20 minutes before going out, reapply, stay covered, in shade, hat, avoid sun at midday

201
Q

What is atopic dermatitis?

202
Q

What causes xerotic skin?

A

normally swelled corneocytes fill with NMF to retain moisture and lipid bilayers prevent water loss between the corneocytes

but in xerotic skin, there is a loss of NMF leading to dry skin and crack development and an abnormal lipid bilayer provides inadequate permeability barrier

203
Q

How do occlusive emollients (with and without humectants) treat xerotic skin?

A

trap moisture in the skin to increase hydration and form an artificial permeability barrier above the stratum corneum

added humectants retain the moisture, further increasing hydration

204
Q

What is the hierarchy of treatments for eczema?

A

manage triggers, emollients

garments, wet wraps, paste bandages
topical calcineurin inhibitors (pimecrolimus cream, tacrolimus ointment)
topical corticosteroids (hydrocortisone, flucinoninde)

antibiotics/antiseptics

sedative antihistamines
UV treatment

systemic treatments

antibiotics

205
Q

What is the difference between lesional and non lesional skin?

A

lesional = clinical inflammation (flare)

non lesional = skin show signs of subclinical inflammation between flares

206
Q

What is proactive treatment for flares?

A

reduces frequency of flares by continually controlling sub clinical inflammation

207
Q

side effects of corticosteroids for atopic dermatitis?

A

skin atrophy, suppression of skin barrier homeostasis, striae, telangiectasia, perioral dermatitis, acne, hypopigmentation, hypertrichosis

208
Q

side effects of calcineurin inhibitors?

A

burning/stinging after application of TCI, less efficacious than TCS, unsubstantiated cancer risk

209
Q

What is done in phototherapy?

A

UVB treatment 3x a week , 10-30 treatment overall
narrow band UVB
photochemotherapy uses psoralens and UVA

210
Q

What systemic therapy can be used for atopic dermatitis?

A

antihistamines e.g. chlorphenamine, hydroxyzine

immune modulators e.g. ciclosporin, azathioprine

211
Q

How does methotrexate treat psoriasis?

A

a dmard, inhibiting metabolism of folic acid, antiproliferative and antiinflammatory, it is hepatotoxic

212
Q

CI of methotrexate?

A

pregnancy, breast feeding, hepatic disease, alcoholism, renal impairment, active infection, live vaccines

213
Q

Treatment of guttate psoriasis?

A

mild-moderate TCS, coal tar, UVB

214
Q

What is acitretin?

A

an oral retinoid used to treat palmoplantar psoriasis, it a vit A derivative and an anti proliferative reducing hyperkeratosis, adjunct to phototherapy

215
Q

Side effects of acitretin?

A

dry lips, eyes, mucosa, hyperlipidemia, disturbed liver function, hyperostosis, teratogenic

216
Q

CI of acitretin?

Phase 2a (15 decks)

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