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Y2 Dermatology > Week 2 > Flashcards

Week 2 Flashcards

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Dermatology Board Prep flashcards
1
Q

What are the chemical mediators that causes pruritus

A

PGE2
IL2
Histamine
Substance P
Acetylcholine

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2
Q

What type of nerve transmits the sense of pruritus to the brain

A

Unmyelinated C fibres

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3
Q

Describe the synergism between PGE2 and histamine

A

PGE2 reduces the threshold of human skin to histamine evoked itching

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4
Q

Different causes of pruritus

A

Pruriceptive
Neuropathic
Neurogeic
Psychogenic

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5
Q

What mediates neurogenic cause of itch

A

Opiates (exogenous or endogenous)

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6
Q

What is pruritoceptive cause of pruritus

A

When something in the skin that triggers the itch e.g. inflammation / dryness

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7
Q

What is neuropathic cause of pruritus

A

Damage to central or peripheral nerves causing itch

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8
Q

What is psychogenic cause of pruritus

A

Psychological causes with no CNS damage

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9
Q

Presentation of acne vulgaris

A

Non-inflammatory lesions: comedones (open or closed)
Inflammatory lesions: papules, nodules, pustules
Cysts
Scarring
Erythema

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10
Q

Difference between papules and pustules

A

Papules are solid raised bumps that are not pus filled whereas pustules are

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11
Q

Difference between pustules and cysts

A

Cysts = multiple pustules joined together to form a larger pus filled cyst

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12
Q

What are open comedones

A

Blackheads

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13
Q

What are closed comedones

A

White heads

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14
Q

Cause of acne vulgaris

A

Increase in sebum production / hyperplasia of sebaceous glands causing occlusion of pores allowing bacterial colonisation hence causing inflammation

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15
Q

What causes hyperplasia of sebaceous glands

A

Increase in androgens

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16
Q

What is considered as mild acne

A

Scattered papules, pustules and comedones

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17
Q

What is considered as moderate acne

A

Numerous papules, pustules
mild atrophic scarring

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18
Q

What is considered as severe acne

A

extensive inflammatory lesions including nodules, cysts
Significant atrophic scarring

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19
Q

Example of atrophic scarring

A

Ice pick scarring - small indentations on the skin due to acne

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20
Q

Why does acne mostly appear during puberty

A

Because during puberty, there is an increase in androgen. Increase in androgens then cause increase in sebum and hyperplasia of sebaceous glands

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21
Q

Describe the distribution of acne vulgaris

A

Reflects sebaceous glands sites
- face
- back
- chest

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22
Q

Management for mild acne

A

Topical benzoyl peroxide + topical clindamycin

Or
topical benzoyl peroxide + topical adapalene

Or
Clindamycin + tetrinoin

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23
Q

Management for moderate acne vulgaris

A

Topical benzoyl peroxide + topical adapalene / Clindamycin + topical tetrinoin / topical benzoyl peroxide + topical clindamycin

Or
Azelaic acid + oral tetracycline

Or
Oral anti-androgen

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24
Q

Examples of topical retinoids

A

adapalene
isotretinoin
tretinoin

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25
Q

What effect does topical retinoid have on the skin

A

Drying effect which removes excess sebum

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26
Q

What effect does topical benzoyl peroxide have on the skin

A

Keratolytic (keratin builds up in acne)
Antibacterial

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27
Q

What are the oral antibiotics used for acne vulgaris

A

Tetracyclines: doxycycline, Lymecycline

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28
Q

Contraindications for tetracyclines

A

Pregnancy
Breastfeeding

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29
Q

What are the oral anti-androgens that females can take to treat moderate acne

A

Oral contraceptive pill
Spironolactone

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30
Q

Why are oral anti-androgens not used in males

A

Due to feminising effects

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31
Q

Management for severe acne

A

Oral isotretinoin

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32
Q

What should patients be aware of when taking oral isotretinoin

A

There will be an initial aggravation of acne before it gets better

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33
Q

Contraindications for oral retinoids

A

Pregnancy
Liver impairment

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34
Q

Side effects of oral retinoids

A

Dry mucous membranes
Hair thinning
Hair loss
Headaches

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35
Q

What 2 things should be monitored when taking oral retinoids and why

A

LFT due to risk of hepatitis
Any changes in mood due to risk of depression

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36
Q

What is rosacea

A

chronic skin condition causing flushing of the forehead, nose, cheeks and chin

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37
Q

Rosacea is more common in females / males

A

Females

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38
Q

Rosacea most commonly affects which age group

A

30-60 years old

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39
Q

Presentation of Rosacea

A

Facial flushing
Rash
- Erythema
- Papules and pustules
- telangiectasia
- Rhinophyma

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40
Q

What is rhinophyma

A

Enlarged red nose, a bulb shape

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41
Q

Facial flushing in rosacea can be exacerbated by

A

Increase in temperature
Alcohol
Spicy foods
Sun exposure
Warm baths

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42
Q

Difference between rosacea and acne

A

Rosacea is not due to inflammation in pilosebaceous unit
Rosacea does not have comedones

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43
Q

Management for rosacea

A

Avoid triggers
Use sun protection creams
1. Topical treatment (brimonidine / metronidazole)
2. Oral therapies (tetracycline / isotretinoin if severe)
Laser therapy (for persistent telangiectasia)
Surgery (for rhinophyma)

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44
Q

Describe the topical therapies for rosacea

A

Topical brimonidine or Ivermectin
Topical metronidazole (antibiotic)

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45
Q

Describe the oral therapies for rosacea

A

Oral tetracycline
Low dose oral isotretinoin for severe rosacea

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46
Q

Rosacea increases risk for infestation of which organism

A

Demodex mites infestation at eyelashes

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47
Q

Laser therapy for rosacea is indicated when

A

Patient has persistent telangiectasia

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48
Q

Complications of rosacea

A

Rhinophyma
Ocular involvement - conjunctivitis, blepharitis (Gritty eyes)

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49
Q

What are lichen disorders

A

Conditions characterised by damage to basal epidermis

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50
Q

Differences between lichen planus and psoriasis

A

Psoriasis is scaly whereas lichen planus isn’t
Psoriasis doesn’t involve the oral cavity whereas lichen planus does

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51
Q

What are the 6 Ps that characterise lesions of lichen planus

A

very Pruritic
Polygonal
Purple
Planar (flat topped)
Papules or Plaques

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52
Q

Symptoms of lichen planus

A

6Ps
Very itchy
Oral involvement
Wickham’s striae
Longitudinal ridging of the nails

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53
Q

How does lichen planus affect the mouth

A

Mucosal ulceration
Wickham’s striae inside of the mouth

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54
Q

What is Wickham’s striae

A

Lacy white lesions

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55
Q

Oral candida also causes white lesions. How can you differentiate it from Wickham’s lesions in Lichen Planus

A

The white lesion in Lichen Planus cannot be wiped off

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56
Q

Describe the distribution of lesions in Lichen planus

A

Flexural distribution - wrists, ankles
Legs

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57
Q

Histological features of lichen planus

A

Irregular sawtooth acanthosis
Cytoid bodies
Inflammatory cells infiltrate at upper dermis
Orthohyperkeratosis

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58
Q

What is orthohyperkeratosis

A

Thickening of stratum corneum (outermost layer) with non-nucleated keratinocytes

so this is not parakeratosis because parakeratosis involves retaining the nuclei

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59
Q

Management for Lichen planus

A

Emollients
Topical steroid
PUVA / UVB phototherapy
Oral steroids if lesions do not resolve after 12 months

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60
Q

What is lichenoid eruption

A

Lichenoid disorder due to medication

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61
Q

Difference between lichen planus and lichenoid eruption

A

Lichenoid eruption affects the trunk, it does not have a flexural distribution
Lichenoid eruption does not usually cause Wickham’s striae
Lichenoid eruption is due to a specific trigger - medications

62
Q

When do symptoms of lichenoid eruption usually occur

A

2 months after starting a medication

63
Q

Drugs that commonly causes lichenoid eruption (BA GPT)

A

Beta blockers
ACEi
Gold
Thiazides
Penicillamine

64
Q

Management for lichenoid eruption

A

Discontinue the drug and use alternative
Topical steroids
Emollients

65
Q

What can cause bullae to form

A

Burn
Eczema
Herpes infection
Immunobullous disorders

66
Q

List the 3 immunobullous disorders

A

Dermatitis herpetiformis
Bullous pemphigoid
Pemphigus Vulgaris

67
Q

What is the general cause of the immunobullous disorders

A

Autoimmune disorders causing damage to adhesion mechanisms in the skin

68
Q

What causes bullous pemphigoid

A

IgG antibodies attacking the hemidesmosomes that anchor the basal cells to basement membrane
Causes interruption of the dermo-epidermal junction

= the pathology is at the DEJ

69
Q

Bullous pemphigoid most commonly occur in

A

Elderly patients

70
Q

Presentation of bullous pemphigoid

A

1) Only pruritus before plaques
2) Itchy erythematous plaques and papules
3) Large deep bullae on erythematous base
4) Erosions when blisters burst

71
Q

Distribution of bullous pemphigoid

A

Proximal limbs
Trunk
Can be localised

72
Q

Investigations for bullous pemphigoid

A

Nikolsky sign - negative
Immunofluorescence
Skin Biopsy

73
Q

What would immunofluorescence show in bullous pemphigoid

A

IgG deposition at basal membrane
Dermal papillae (thin top layer of dermis) projecting into bulla

74
Q

What would immunofluorescence show in bullous pemphigoid

A

IgG deposition at basal membrane
Dermal papillae (thin top layer of dermis) projecting into bulla

75
Q

Management of bullous pemphigoid

A

High potency topical steroids
Oral tetracycline antibiotic
Oral steroids
Immunosuppressive drugs

76
Q

Which high potency topical steroid is used for bullous pemphigoid

A

Dermovate

77
Q

Which oral tetracycline antibiotic is used in bullous pemphigoid

A

Doxycycline
Lymecycline

78
Q

Which oral steroid is used for bullous pemphigoid

A

Oral prednisolone

79
Q

What should you monitor when giving oral steroids

A

Glucose level
Blood pressure

80
Q

Why should you monitor glucose level when giving oral steroids

A

Because steroids act like glucagon where they increase blood sugar

81
Q

How should you adjust the dose of oral steroid for bullous pemphigoid

A

Reduce quickly at first to 15-20mg per day then more slowly afterwards.
Increase the dose if blisters start again then reduce again when blisters resolve

82
Q

Cause of pemphigus vulgaris

A

IgG antibodies depositing in epidermis and attacking the desmosomes between keratinocytes in the epidermis causing the cells to separate

= pathology is at epidermis

83
Q

What is the protein that maintains desmosomal attachments between keratinocytes

A

Desmoglein 3

84
Q

Difference between pemphigus vulgaris and bullous pemphigoid (bullous pemphigoiD and pemphiguS)

A

Bullous pemphigoid pathology is at Dermo-epidermal junction whereas pemphigus vulgaris is within epidermis

Bullous pemphigoid- deep blisters
pemphigus vulgaris- superficial blisters

Bullous pemphigoid Nikolsky’s sign - negative
Pemphigus vulgaris Nikolsky’s sign - positive

Bullous pemphigoid does not affect mucosal membranes whereas pemphigus vulgaris does

85
Q

Presentation of pemphigus vulgaris

A

Thin roofed, fragile lesions
Superficial lesions
Raw areas left after blisters burst

86
Q

Distribution of pemphigus vulgaris

A

Face
Scalp
Axillae
Groin
Mucosa

87
Q

Which mucosal membranes are commonly affected by pemphigus vulgaris

A

Oral mucosa
Eyes
Genitals

88
Q

What is at an increased risk due to rupture of blisters in pemphigus vulgaris

A

Infection because the rupture of blisters leave raw areas = ineffective skin barrier

89
Q

Investigations for pemphigus vulgaris

A

Nikolsky’s sign
Immunofluorescence
Skin biopsy

90
Q

Nikolsky’s sign in pemphigus vulgaris is

A

Positive

91
Q

Immunofluorescence of pemphigus vulgaris will show

A

IgG antibodies deposited within the epidermis
Chicken wire appearance

92
Q

Histology of pemphigus vulgaris

A

Intra-epidermal blister
Acantholysis

93
Q

Management of pemphigus vulgaris

A

Topical steroids
Oral steroids
Immunosuppressive agents

94
Q

Bullous pemphigoid and pemphigus vulgaris are both part of which type of hypersensitivity

A

Type 2 - IgG or IgM mediated

95
Q

What is dermatitis herpetiformis

A

Autoimmune bullous disorder associated with coeliac disease

96
Q

Cause of dermatitis herpetiformis

A

IgA antibodies targeting gluten and causing immune complexes to form in dermal papillae -> triggers inflammation -> sub epidermal blisters

97
Q

Presentation of dermatitis herpetiformis

A

VERY itchy lesions
Symmetrical lesions on erythematous base

98
Q

Distribution of dermatitis herpetiformis

A

Buttocks
Extensor surfaces - inner elbow, front of knee

99
Q

Investigations for dermatitis herpetiformis

A

Serum anti TTG IgA antibodies
Immunofluorescence
Skin biopsy

100
Q

2% of Coeliac patients have IgA deficiency. How should you test for Coeliac if the patient has IgA deficiency

A

Do Serum Anti-TTG IgG instead

101
Q

What would immunofluorescence show in dermatitis herpetiformis

A

IgA deposits in dermal papillae

102
Q

What would histology show in dermatitis herpetiformis

A

Sub-epidermal blisters

103
Q

Management of dermatitis herpetiformis

A

Treat Coeliac - gluten free diet

104
Q

What is photosensitivity

A

Group of disorders that result from exposure to normal levels of UV light

105
Q

Cause of photosensitivity

A

Multifactorial - genetics, environment, skin type

106
Q

What environmental factors may cause photosensitivity

A

Use of photosensitive drug
Intensity of UV light

107
Q

How many skin types are there in Fitzpatrick skin type

A

6

108
Q

Which skin type has higher tendency to be photosensitive

A

Skin type 1

109
Q

Describe skin type 1

A

Very fair skin colour
Always burns
Never tans

110
Q

People with what colour of hair tends to be skin type 1 and why

A

Red hair
Because those people have less eumelanin and more pheomelanin

111
Q

2 types of melanin

A

Eumelanin
Pheomelanin

112
Q

Which gene controls which melanin is produced

A

MC1R (Melanocortin 1 receptor gene)

113
Q

What happens when MC1R is switched on

A

Switches from producing pheomelanin to eumelanin

114
Q

Function of pheomelanin

A

Causes yellowish to reddish colour
Gives pinkish fairer skin type
Does not absorb UV light hence does not protect skin from UV light damage

115
Q

What is eumelanin

A

Type of melanin that gives dark pigmentation to skin and hair

116
Q

Where is pheomelanin most abundant in

A

Nipples
Lips
Vagina
Glans of penis
Skin and hair (causes red hair and fair skin)

117
Q

People with type 1 skin colour are at risk of

A

Skin cancer
Photosensitivity

118
Q

Describe skin type 6

A

Black
Never burns
Always tans

119
Q

What is xeroderma pigmentosum

A

Genetic condition characterised by extreme photosensitivity

120
Q

Inheritance pattern of xeroderma pigmentosum

A

Autosomal recessive

121
Q

What causes xeroderma pigmentosum

A

Deficiency in DNA repair mechanism in skin hence unable to repair the DNA damage caused by UV light

122
Q

Xeroderma pigmentosum increases the risk for

A

Skin cancer
Severe sunburn
Accelerated photoaging
Ocular damage

123
Q

Management for xeroderma pigmentosum

A

Sun avoidance and protection
Vitamin D supplements

124
Q

Life expectancy for patients with xeroderma pigmentosum

A

Teenage - young adults
Most die young due to skin cancer

125
Q

What is porphyria

A

Group of photosensitivity disorders resulting from defects in enzymes required to produce adequate amount of haem or unable to break down porphyrin resulting in accumulation of porphyrins

126
Q

Porphyrin is required in

A

Haemoglobin

127
Q

Conditions in porphyria

A

Porphyria Cutanea Tarda
Erythropeotic protoprophyria

128
Q

Porphyria Cutanea tarda is caused by deficiency in ___ causing ____

A

Uroporphyrinogen decarboxylase enzyme causing accumulation of uroporphyrinogen

129
Q

What factors can cause deficiency in uroporphyrinogen decarboxylase hence PCT

A

Genetics
Alcohol (50% case)
Oestrogen replacement

130
Q

Symptoms of PCT

A

Painful blisters on sun exposed sites
Scarring and Hyperpigmentation after blisters heal
Hypertrichosis

131
Q

What is hypertrichosis

A

Excessive hair growth

132
Q

Where is hypertrichosis mainly seen in PCT

A

Top of cheeks

133
Q

Where are symptoms of PCT commonly seen

A

Dorsum of hands

134
Q

PCT is associated with which conditions

A

Hepatitis
Alcohol abuse
Haemochromatosis

135
Q

Investigations for PCT

A

Urinary porphyrin
Skin biopsy

136
Q

Management for PCT

A

Sun avoidance
Treat hepatitis / alcohol misuse/ haemochromatosis
Stop oestrogen replacement therapy / find alternative

137
Q

What causes erythropeotic protoporphyria

A

Ferrochelatase deficiency causing accumulatino of protoporphyrin IX

138
Q

Inheritance pattern of erythropeotic protoporphyria

A

Autosomal dominant

139
Q

Erythropeotic protoporphyria most commonly seen in

A

Children

140
Q

Symptoms of erythropeotic protoporphyria

A

Burning and itching with sun exposure
Child screaming when out in the sun

141
Q

What is seborrheic dermatitis

A

dermatitis affecting areas of skin rich in sebaceous glands

142
Q

Cause of seborrheic dermatitis

A

inflammatory reaction to the proliferation of Malassezia furfur (a yeast normally found on the skin.)

143
Q

Risk factors for seborrheic dermatitis

A

Family history
Oily skin
Immunosuppression (such as HIV)
Neurological and psychiatric diseases (such as Parkinson’s Disease or Depression)
Stress

144
Q

Presentation of seborrheic dermatitis

A

Greasy, flaky scales
Ill defined margins
Erythematous base

145
Q

Where does seborrheic dermatitis usually present on

A

nasolabial folds
posterior auricular skin
scalp

146
Q

The distribution of seborrheic dermatitis reflects

A

sebum rich areas

147
Q

What is a term used to describe mild seborrheic dermatitis

A

Dandruff

148
Q

Management of seborrheic dermatitis

A

Zinc Pyrithione shampoo
Ketoconazole shampoo or cream
Short course of topical corticosteroid

149
Q

What is the other term for infantile seborrheic dermatitis

A

Cradle cap

150
Q

Presentation of infantile seborrheic dermatitis

A

diffuse, yellow, greasy scales
No underlying erythema

151
Q

Where is infantile seborrheic dermatitis most commonly found on

A

Scalp

152
Q

management of infantile seborrheic dermatitis

A

topical emollient, commonly olive oil
scales are brushed off gently
use normal baby shampoo

Y2 Dermatology (5 decks)

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