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4. Senior Block- Special Senses > Dermatology > Flashcards

Dermatology Flashcards

1
Q

Give 4 functions of skin

A

Barrier between external world and body contents
Protection against mechanical, chemical, osmotic, thermal and UV damage as well as microbial invasion
Synthesis of vitamin D
Regulation of body temperature
Psychosexual communication
Sensory organ- touch, temperature, pain

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2
Q

What cells are present in the epidermis?

A

Keratinocytes
Melanocytes
Langerhans cells
Merkel cells

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3
Q

Give the layers of the epidermis and their function

A

Stratum Basale- mitosis of keratinocytes
Stratum spinosum- keratinocytes joined together
Stratum granulosum- cells secrete lipids
Stratum lucidum- cells lose nuclei and keratin production increases
Stratum corneum- cells lose all organelle, keratin produced

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4
Q

What cells and structures are found in the dermis?

A 
Fibroblasts
Mast cells 
Blood vessels 
Sensory fibres
Hair follicles
Sebaceous glands
Sweat glands
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5
Q

What is the name of the muscle attached to hair follicles that allows them to stand up?

A

Arrector pili

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6
Q

What is the function of a skin eccrine gland?

A

Thermoregulation

Releases clear, odourless sunstance

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7
Q

What is the function of a skin apocrine gland?

A

Located in axilla and groin. Releases products which are broken down by bacteria and so are odorous.

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8
Q

Give 10 things to ask in a dermatology history

A 
Initial appearance
Evolution of lesion 
Symptoms - itching, pain, discharge 
Aggravating and relieving factors
Previous and current treatments
Recent contact with irritants
Recent travel 
Sunburn history 
Immunisation history 
Family history of skin cancers
History of atopy 
Occupation risk 
Pets 
Current medications and allergies 
Impact on QoL
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9
Q

What factors are important to look at when examining the skin?

A 
Shape of lesion 
Pattern of lesions 
Border
Surface 
Distribution 
Elevation 
Colour 
Temperature
Photosensitive
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10
Q

What is a macule?

A

Flat, non-palpable change in skin colour

<0.5mm

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11
Q

What is a patch?

A

Flat, non-palpable change in skin colour

>0.5cm

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12
Q

What is a vesicle?

A

Fluid in upper layers of the skin

<0.5cm

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13
Q

What is a blister?

A

Fluid in upper layers of the skin

>0.5cm

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14
Q

What is a pustule?

A

A vesicle filled with pus

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15
Q

What is a bulla?

A

> 10mm diameter, fluid filled lesion below the epidermis

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16
Q

What is a papule?

A

Raised area

<0.5cm

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17
Q

What is a plaque?

A

Raised area >0.5cm

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18
Q

What is a nodule?

A

Mass or lump >0.5cm

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19
Q

What is a callus?

A

Hyperplastic epidermis

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20
Q

What is a wheal?

A

Dermal oedema

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21
Q

What is an ulcer?

A

Full thickness skin loss

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22
Q

What is atrophy?

A

Thinning of the epidermis

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23
Q

What is scale?

A

Thin piece of horny epithelium

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24
Q

What is excoriation?

A

Scratch marks

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25
Q

What is lichenification?

A

Thickening of the epidermis with exaggerated skin markings and scratching

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26
Q

What is purpura?

A

Blood in the skin- non-blanching

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27
Q

What is erythema?

A

Red skin due to local vasodilation

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28
Q

What are striae?

A

Stretch marks

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29
Q

Give 3 risk factors for benign melanocytic naevi

A

Family history
Sunburn
Excess sun exposure
Fair skin

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30
Q

What is the pathophysiology of the development of benign melanocytic naevi?

A

Junctional naevi: flat, evenly pigmented naevi where melanocytes collect along the basal layers of the epidermis

Compound naevi: melanocytes migrate from the epidermis to the demis and the moles evolve into raised, evenly pigmented dome shaped naevi.

Intradermal naevi: epidermal component is lost and the moles change to pale brown papules before disappearing

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31
Q

How are benign melanocytic naevi managed?

A

No need to remove
Wear suncream
Watch for mole changes

Can remove for cosmetic reasons or trauma or suspicion of melanoma

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32
Q

What is a seborrhoeic keratosis?

A

Benign, brown, warty lesions usually on the back, chest and face. Start as small, rough papules and then thicken and become wart-ike. Look stuck on

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33
Q

What is the management of seborrhoeic keratoses?

A

Leave them alone
Cryotherapy
Curettage removal + biopsy

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34
Q

What is an epidermal cyst?

A

Cyst full of keratin with the cyst lining made of epidermal cells. Common on face, neck, genital skin and upper trunk. Small, yellow/white dome-shaped lumps

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35
Q

Who do epidermal cysts affect?

A

Young to middle age adults

Common in acne

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36
Q

How are epidermal cysts managed?

A

Leave alone
Can surgically remove
Antibiotics if infected

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37
Q

What is a pilar cyst?

A

Cyst full of keratin but lining made up of cells found at the root of hairs. Commonly found on the scalp.

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38
Q

What is a dermatofibroma?

A

Overgrowth of fibrous tissue in the dermis thought to appear after a minor injury to the skin. Firm rubbery bumps within the skin. Common on lower legs.

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39
Q

How is a dermatofibroma managed?

A

Spontaneous resolution
Removal under LA
Cryotherapy
Intralesional steroid injections

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40
Q

Describe a cutaneous neurofibroma

A

Circumscribed superficial soft brown/skin coloured nodules with buttonhole invagination.

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41
Q

Describe a subcutaneous neurofibroma?

A

Circumscribed soft brown/skin coloured nodules with buttonhole invagination. Deep in the skin so causes tenderness

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42
Q

What is a plexiform neurofibroma?

A

Bag-like mass found within the skin. Invasive tumours which involves all layers of the skin, muscle, bone and blood vessels.

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43
Q

What is a cafe au lait patch and what condition do they suggest?

A

Well-defined, oval, light brown patches >0.5cm

Neurofibromatosis if >5 patches

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44
Q

What is a keratoacanthoma?

A

Rapidly growing lesion that develops in sun exposed areas. Initially appears as a small pimple or boil and then becomes a firm lump with a horn or scale in the centre which can erupt and form a crater

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45
Q

How is a keratoacanthoma managed?

A

Look very similar to SCC!

So excise and biopsy

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46
Q

What is a strawberry naevus?

A

Haemangioma which occurs in infancy. Begins as a small, red lesion which grows into a dimpled plaque. Grow until age 3-4 and then regress.

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47
Q

Give 4 risk factors for strawberry naevus development

A

Low birth weight
Prematurity
Multiple gestation
Chorionic villus sampling

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48
Q

How is a strawberry naevus managed?

A

Do nothing
Topical beta blocker
Surgical excision –> very vascular structure so be very careful

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49
Q

What is a pyogenic granuloma?

A

Overgrowth of capillaries in the skin which occur after minor damage to the skin.
Commonly found on the fingers, scalp, mouth and gums
Red rapidly growing nodules which actively bleed on minor trauma

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50
Q

How is a pyogenic granuloma managed?

A

Cryotherapy
Curettage
Creams –> topical timolol and steroids

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51
Q

Give 3 risk factors for actinic (solar) keratoses

A

Excess sunbathing
Sunbed use
Outdoor work
Type 1 skin

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52
Q

What is the pathophysiology of actinic (solar) keratoses

A

Sun induced dysplastic intra-epidermal proliferation of atypical keratinocytes. Skin becomes thicker

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53
Q

What are the clinical features of actinic (solar) keratoses?

A

Crumbly, yellow, scaly, crusty lesions
Rough feeling
Surrounding skin- blotchy, freckled, wrinkled
Sun exposed areas

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54
Q

How are actinic (solar) keratoses managed?

A 
Sun protection 
Cryotherapy 
Surgical removal under LA
Creams --> 5-fluorouracil, diclofenac, Imiquimod
Photodynamic therapy

Need treating as can turn into SCC

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55
Q

What is Bowen’s disease?

A

Squamous cell carcinoma in situ

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56
Q

Give 4 risk factors for Bowen’s disease

A

Long term sun exposure
Immunosuppression
Post radiotherapy
HPV infection on genitals

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57
Q

What are the clinical features of Bowen’s disease?

A

Slowly enlarging red, scaly plaque with flat edge

Found on sun exposed skin

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58
Q

How is Bowen’s disease managed?

A

5% progress to SCC

Cryotherapy 
Curettage
Excision 
Creams --> 5-fluorouracil, Imiquimod 
Photodynamic therapy 
Radiotherapy
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59
Q

Give 4 pieces of advice you could give to a patient about avoiding sun damage to the skin

A

Avoid the sun between 11am and 3pm
Wear protective clothing- hats, long sleeves
Apply suncream >factor 30 and reapply regularly
Avoid sunbeds
Check unusual lesions with a GP quickly
Ask GP to monitor vitamin D levels

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60
Q

Give 4 predisposing factors for basal cell carcinoma

A 
Sun exposure
Immunosuppression 
Tanning beds
Type 1 skin 
Radiotherapy 
Previous BCC
FHx of BCC
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61
Q

What is the pathophysiology of basal cell carcinoma?

A

Cancer of the basal cells in the epithelium. Highly localised and does not spread but can invade local tissue

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62
Q

Describe a typical basal cell carcinoma lesion

A 
Nodule with raised pearly edges 
Central ulceration 
Visible surface telangiectasia
May bleed, crust over, ooze
Will not heal 
Found on sun exposed areas
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63
Q

How is a basal cell carcinoma managed?

A

Wide excision
Curettage and electrodesiccation
Mohs surgery –> microscopy done at time of surgery
Radiotherapy
Photodynamic therapy –> very early cancer

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64
Q

Give 4 risk factors for squamous cell carcinoma

A 
sun exposure
Immunosuppression 
HPV infection 
Type 1 skin 
Albinism 
History of sunburn 
Actinic keratoses
Xeroderma pigmentosum
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65
Q

What is the pathophysiology of squamous cell carcinoma?

A

UV light causes mutations in the DNA of keratinocytes in the epidermis resulting in cancerous changes

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66
Q

Give 4 clinical features of squamous cell carcinoma

A

Scaly nodule with red inflamed base
Presistanty ulcerated
Sore, tender, bleeds
Found on sun exposed areas

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67
Q

How is squamous cell carcinoma managed?

A

Excision

Mohs surgery

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68
Q

Where do squamous cell carcinomas tend to metastasise to?

A

Lymph nodes

Surrounding tissues

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69
Q

Give 4 risk factors for malignant melanoma

A 
Sun exposure
Sun burn 
FHx of MM
Advanced age 
Immunosuppression 
Type 1 skin 
>50 benign melanocytic naevi
Previous melanoma
Sunbed use
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70
Q

What are the 4 types of malignant melanoma?

A

Superficial spreading melanoma (70%)
Nodular melanoma (15%) - most aggressive type, metastasise early
Acral lentiginous melanoma (10%)- Black and Asian populations- soles and palms
Lentigo maligna melanoma (5%)

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71
Q

What is the A-F of assessing potential melanomas?

A 
Asymmetry 
Borders (irregular, poorly defined) 
Colour variation 
Diameter (>7mm)
Evolution 
Funny looking --> mole looks different to others around it
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72
Q

What is the Breslow score in melanoma management?

A

Measurement of how far melanoma cells have spread down from the surface in mm

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73
Q

How are malignant melanomas staged?

A

Using TNM (with help of Breslow for T score)

TNM translated to Stage 0-4

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74
Q

Briefly describe stages 0-4 of malignant melanoma

A

Stage 0= in situ
Stage 1= low Breslow score, not ulceration
Stage 2= high Breslow score +/- ulcerated lesion
Stage 3= nodal involvement
Stage 4= metastatic disease

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75
Q

How are malignant melanomas managed?

A

Stage 0 = wide local excision
Stage 1+2= wide local excision + sentinal node biopsy
Stage 3= wide local excision +/- lymoh node dissection +/- radiotherapy +/- biological therapy
Stage 4= chemotherapy, radiotherapy, surgery, biological therapy (palliative)

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76
Q

Give 4 common sites for malignant melanoma to spread to

A 
Lungs 
Liver 
Bone 
Brain 
Abdomen 
Lymph nodes
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77
Q

Where are melanomas most commonly found on men and women?

A

Men: back
Women: shins

78
Q

What is anaphylaxis?

A

Severe and life-threatening reaction to a trigger such as nuts, drugs, insect stings, GA, latex, milk.

79
Q

How does anaphylaxis manifest in the skin?

A

Pruritus
Erythema
Urticaria
Angioedema

80
Q

What is angioedema?

A

Swelling of the deep dermis usually in the hands, feet, orbits, lips, tongue and genitals

81
Q

How is anaphylaxis managed?

A

Remove trigger
Use Epipen
Recovery position
A-E resuscitation

82
Q

What is erythroderma?

A

Intense and widespread erythema due to inflammatory skin disease

83
Q

Give 4 causes of erythroderma

A 
Idiopathic
Psoriasis
Atopic dermatitis
Cutaneous T cell lymphoma 
HIV infection 
Drug eruption (Sulphonamides, Alopurinol, Carbamazepine, Gold)
84
Q

Give 4 systemic complications of erythroderma

A

Widespread vasodilation causes erythema

Heat loss, Fluid loss, Electrolyte imbalance, Skin infections, Hypoalbuminaemia

85
Q

How is erythroderma managed?

A

Correct systemic problems
Treat underlying cause
Bed rest

86
Q

What is necrotising fasciitis?

A

Rapidly progressive skin infection caused by Group A streptococcus and S.aureus.

87
Q

Describe a necrotising fasciitis lesion

A

Painful, cyanotic, blistered, necrotic, deep gangrene

88
Q

How is necrotising fasciitis managed?

A

Emergency!
IV Abx
Fluids
Surgical debridement immediately

89
Q

What is Toxic Epidermal Necrolysis (TEN)? Give 3 drug causes

A

Life-threatening condition with widespread death of the epidermis as a result of apoptosis induced by a toxin.

Causes –> drug reaction- sulphonamides, penicillins, allopurinol, anti-epileptics, cephalosporins, NSAIDs

90
Q

Give 3 clinical features of TEN

A

Flu like symptoms
Widespread painful erythema
Necrosis of large sheets of epidermis

91
Q

How is TEN managed?

A 
ICU
Pain relief
Fluids 
IV immunoglobulins 
Protect skin
92
Q

What is Stevens-Johnson Syndrome?

A

Severe erythema multiforme with widespread skin involvement

93
Q

Give 2 clinical features of Stevens-Johnson Syndrome

A

Painful erythematous macules which become target lesions (central necrosis with ring of erythema)
Mucosal ulceration

94
Q

Give 4 drug causes of Stevens-Johnson Syndrome

A

Sulphonamides
Anti-epileptics
Penicillins
NSAIDs

95
Q

Give 4 predisposing factors for Eczema Herpeticum

A 
Inflammatory skin condition 
Severe eczema 
Eczema from infancy 
Skin trauma
Cosmetic procedures (lasers, skin peels)
96
Q

What is the pathophysiology of Eczema Herpeticum?

A

Herpes simplex virus type 1 infects large areas of skin (often spread from a small cold sore)

97
Q

Describe the lesions seen in Eczema Herpeticum

A

Starts with groups of small blisters which then increase in number of 7-10 days. Contain a clear fluid which develops into pus. Can weep or bleed. Itchy

98
Q

How is Eczema Herpeticum managed?

A

IV Acyclovir
Topical antibiotics for secondary infection cover
Normal eczema treatments- emollients
Avoid contact with others- contagious

Refer to ophthalmology due to risk of eye involvement

99
Q

Describe a DIC rash

A 
Petechiae
Purpura
Ecchymosis
Blood oozes from wounds/lines 
Purpura fulminans- extensive skin necrosis
100
Q

Give 5 potential triggers for Atopic eczema

A 
Soaps
Shampoos
Allergens --> dust, fur, pollen
Environment --> cold/dry weather, damp
Wool or synthetic fabrics
Skin infections 
Hormonal changes 
Stress
101
Q

What are the clinical features of atopic eczema?

A

Itchy, erythematous dry scaly patches
Common on face and in flexures
Acute lesions are erythematous, vesicular and weepy
Nail pitting and rail ridging
Chronic scratching
Usually develops in early childhood and resolves as a teenager

102
Q

How is atopic eczema managed?

A 
Avoid triggers
Frequent emollient use 
Patient and family education 
Topical steroids
Topical tacrolimus or pimecrolimus (immunomodulators) 
Antihistamines 
Antibiotics/antivirals for secondary infections 
Phototherapy 
Oral immunosuppressants
103
Q

Give 3 examples of secondary viral infections from atopic eczema

A

Molluscum contagiosum
Viral warts
Eczema herpeticum

104
Q

What is contact dermatitis?

A

Eczema triggered by contact with an irritant. Reaction will occur within a few hours of contact and usually affects the hands and face.

105
Q

What are the clinical features of discoid eczema?

A
  1. Group of small red spots
  2. Large circular red patch
  3. Swollen, blistered, ooze fluid, itchy at night
  4. Dry, crusty, cracked, flaky skin
106
Q

What is the pathophysiology of venous eczema?

A

Valves are incompetent so venous drainage is reduced. Increased pressure in leg veins leads to damage to overlying skin which triggers inflammation.

107
Q

Give 4 risk factors of venous eczema

A 
Obesity 
Immobility 
Leg swelling
Varicose veins 
Hx of DVT
Hx of cellulitis
108
Q

What are the clinical features of venous eczema?

A

Lower legs
Itchy, scaly red spots
Weeping and crusting

Atrophie blanche- white patches of thinning and scarring
Lipodermatosclerosis- thinning of large areas of skin
Leg ulcers

109
Q

What is the management of venous eczema?

A 
Weight loss
Raise feet up 
Be more mobile 
Avoid trauma to legs 
Bandaging and compression stockings 
Topical emollients
110
Q

What is the pathophysiology of psoriasis?

A

Hyperproliferation of keratinocytes in the epidermis leading to proliferation and dilation of blood vessels in the dermis and an infiltration of inflammatory cells.

111
Q

Give 5 potential triggers of psoriasis

A 
Stress
Skin infections 
Skin trauma
Drugs (lithium, NSAIDs, Beta blockers, antimalarials)
Alcohol 
Smoking 
Obesity 
Climate
112
Q

Describe how chronic plaque psoriasis presents

A

Symmetrical well-defined red plaques with silvery scale on extensor aspects of the elbows, knees, scalp and sacrum

113
Q

Describe how flexural psoriasis presents

A

Plaques in moist flexural areas eg. axilla, groin and submammary area. Symmetrical distribution. Less scaly

114
Q

Describe how guttate psoriasis presents

A

Large numbers of small plaques <1cm over the trunks and limbs. Seen in young patients after a streptococcal infections. Lasts 3-4 months

115
Q

Describe how pustular psoriasis presents

A

Yellow brown pustules within plaques on the palms and soles

116
Q

Describe how generalised psoriasis presents

A

Entire body covered in erythematous or pustular plaques with systemic upset.

Can be triggered by rapid removal of steroids

117
Q

Describe the nail changes which occur in psoriasis

A

Pitting
Onycholysis
Thickening
Subungual hyperkeratosis

118
Q

What joint condition can also present with symptoms of psoriasis?

A

Psoriatic arthritis

Seronegative

119
Q

How is psoriasis managed?

A

Conservative- weight loss, stop smoking, education
Topical- corticosteroid, vitamin D analogue
Phototherapy
Oral- methotrexate, ciclosporin, acitretin
Biological therapies- Infliximab, Adalimumab, Etanercept

120
Q

What is the pathophysiology of acne vulgaris?

A
  1. Basal keratinocyte proliferation in pilosebaceous follicles
  2. Increased sebum production
  3. ‘Propionibacterium acnes’ colonisation
  4. Inflammation
  5. Comedones block secretions and so papules, nodules, cysts and scars form.
121
Q

What are the clinical features of acne vulgaris?

A 
Open (blackhead) and closed (whitehead) comedones
Papules 
Pustules 
Nodules 
Cysts 
Commonly on face, chest and back
122
Q

How is mild acne managed?

A

Topical benzoyl peroxide
Topical retinoid
Topical antibiotics

123
Q

How is moderate acne managed?

A

Topical benzoyl peroxide + Topical antibiotics
Oral antibiotics
COCP for girls

124
Q

How is severe acne managed?

A

Isotretinoin

125
Q

Give 4 side effects of isotretinoin

A 
Teratogenic - girls need monthly pregnancy tests
Increased cholesterol 
Deranged LFTs 
Dry eyes, mouth, skin 
Depression 
Muscle pains
126
Q

Give 3 predisposing factors for cellulitis?

A

Immunosuppression
Open wound
Leg ulcers/oedema
Minor skin injury

127
Q

What is cellulitis?

A

Rapidly spreading local infection of the deep dermis and subcutaneous tissue. Caused by S. aureus and Group A Streptococcus

128
Q

What is erysipelas?

A

Superficial skin infection of dermis and upper subcutaneous tissue. Caused by Group A streptococcus

129
Q

Describe how cellulitis will present

A

Commonly on the legs
Local inflammation- redness, swollen, hot, painful
+/- purulent exudate
Poorly defined edges (cellulitis)
Well defined edges (erysipelas)
Lymphadenitis
Systemically unwell- fever, rigors, malaise

130
Q

How is cellulitis managed?

A

Bed rest
Analgesia
Penicillin based antibiotics (Flucloxacillin, Benzylpenicillin) oral/IV
Surgical debridement

131
Q

What is an emergency complication of cellulitis?

A

Necrotising fasciitis

132
Q

What is folliculitis?

A

Localised inflammation of a hair follicle

133
Q

Give 3 infectious causes of folliculitis

A

S. aureus
P. aeruginosa
Candida albicans

134
Q

Give 3 non-infectious causes of folliculitis

A

Ingrown hair, friction, follicular trauma, occlusion

135
Q

How does folliculitis present?

A

Tender papules or pustules at the site of hair follicles

136
Q

How is folliculitis managed?

A

Hygiene measures
Antibacterial soap
Warm compress
Topical mupirocin

137
Q

What are furuncles and carbuncles?

A 
Furuncle= deep folliculitis with abscess in subcutaneous tissue 
Carbuncle= confluent folliculitis, abscess and skin necrosis
138
Q

Give 5 predisposing factors for Impetigo infection

A 
2-6 years old
Developing country 
Underprivileged background 
Warm and humid climate 
Atopic dermatitis 
Diabetes
Immunocompromised
139
Q

What pathogen causes bullous impetigo?

A

S. aureus

140
Q

What pathogen causes non-bullous impetigo?

A

S. aureus or Group A streptococci

141
Q

How does non-bullous impetigo present?

A
  1. Small vesicles surrounded by erythema
  2. Rupture of vesicles
  3. Oozing secretion which dries
  4. Honey coloured crust
  5. Heals without scaring

Found on face around nose and mouth + extremities

142
Q

How does bullous impetigo present?

A

Vesicles grow to form large, flaccid bullae which rupture and form thin brown crusts
Sloughing of the skin, trunk and upper extremities

143
Q

How is impetigo managed?

A

Antibacterial washes- chlorhexidine
Non-bullous= topical Abx- mupirocin, retapamulin
Bullous= cephalexin

Need antibiotics for 24hrs before returning to school

144
Q

Describe the skin presentations of primary, secondary and tertiary syphilis

A

Primary= Chancre- solitary raised papule on the genitals which becomes a painless, firm ulcer with indurated borders and a smooth base. Resolves in 3-6 weeks

Secondary=
Polymorphic rash= non-pruritic macular rash on trunk, extremities, hands and soles
Condylomata lata= broad based, wart like papular erosions in anogenital region

Tertiary= Gumma- destructive granulomatous lesions with a necrotic centre that tend to ulcerate

145
Q

What is the pathophysiology of staphylococcal scalded skin syndrome?

A

Staph aureus infection produces exfoliative toxins which cleave the granular level of the epidermis, causing sheets of skin to slough off

146
Q

How does staphylococcal scalded skin syndrome present?

A

Affects infants and young children
First 24hrs= fever, malaise, irritability, skin tenderness, diffuse erythema
24-48 hours= widespread sloughing off of the skin leaving a scalded appearance. Flaccid, easily ruptured bullae form. Painful lesions, cracking, crusting

147
Q

How is staphylococcal scalded skin syndrome managed?

A

IV Abx= penicillinase resistant penicillin eg. nafcillin
Analgesia
Fluids
Emollients

148
Q

What are the two genotypes of herpes simplex virus?

A

Herpes simplex type 1

Herpes simplex type 2

149
Q

What is the pathophysiology of herpes simplex virus?

A

Transmitted via direct contact with mucosal tissue or secretions from an infected person

  1. Inoculation= virus enters body
  2. Neurovirulence= virus invades, spreads and replicates in nerve cells
  3. Latency= virus remains dormant in ganglion neurons
  4. Reactivation= triggered by stress, trauma, immunodeficiency (clinical features)

Dissemination= infection spreads to unusual sites eg. lungs, GI, eyes. Occurs in immunodeficiency or pregnancy

150
Q

How does labial herpes simplex present?

A

24hrs before= pain, tingling, burning

Recurring, erythematous vesicles which turn into painful ulcerations on the oral mucosa and lip borders

151
Q

How does genital herpes present?

A

Mostly asymptomatic

Rednes, swelling, tingling, pain and pruritus on genitals. Painful lymphadenopathy. Unusual vaginal discharge

152
Q

How is herpes simplex treated?

A

Labial- self limiting

Genital- oral acyclovir for 7 days, hygiene measures, abstain from sex until lesions clear

153
Q

What is erythema multiforme?

A

Rare, acute hypersensitivity reaction triggered commonly by a herpes simplex infection.

Other triggers= fungal infections, NSAIDs, penicillins, barbiturates, immunisations

154
Q

How does erythema multiforme present?

A

Target lesions (symmetrical- hands, feet)
Fever
Myalgia
Arthralgia

155
Q

How is erythema multiforme managed?

A 
Self limiting in 1 month 
Stop drug cause 
Analgesia 
Antihistamines 
Topical steroids
156
Q

Give 2 risk factors for HPV infection

A

Damaged skin/mucous membranes
Immunodeficiency
Genital HPV= unprotected sex, high number of sexual partners, early first sexual encounter

157
Q

Describe the appearance and associated symptoms of anogenital warts

A

Exophytic, cauliflower-like lesions that cause pruritus, tenderness and bleeding
Found on anus, penis, vulva, urethra and cervix

158
Q

Describe the appearance and associated symptoms of common warts

A

Skin coloured rough scaly plaques on elbows, knees and fingers

159
Q

Describe the appearance and associated symptoms of plantar warts

A

Rough hyperkeratotic lesions on sole of foot, painful when walking

160
Q

Describe the appearance and associated symptoms of flat warts

A

Small flat patches or plaques on hands, face or shins

161
Q

How are anogenital warts managed?

A

Cryotherapy

Local topical treatment- Fluorouracil, Imiquimod

162
Q

How are common warts managed?

A

Watch and wait
Cryotherapy
Salicylic acid

163
Q

How are plantar warts managed?

A

Wart paint

Cryotherapy

164
Q

Give 4 predisposing factors for molluscum contagiosum

A 
Male 
<5 years old
Warm and humid climate 
Immunosuppression 
Atopic dermatitis
Crowded living conditions
165
Q

What do molluscum contagiosum lesions look like?

A

Non-tender, flesh coloured pearly dome-shaped papules with central depression
2-5mm in diameter

166
Q

Where do children commonly experience molluscum contagiosum?

A

Face
Trunk
Popliteal fossa
Antecubital fossa

167
Q

Where do adults commonly experience molluscum contagiosum?

A

Lower abdomen
Groin
Genitalia
Proximal thighs

168
Q

How is molluscum contagiosum managed?

A

Spontaneous resolution in 6-9 months
Cryotherapy
Curettage

169
Q

What pathogen causes chickenpox?

A

Varicella zoster virus

170
Q

Describe the clinical features of chickenpox

A

Prodrome= 1-2 days before, fever, malaise

Exanthem phase= 6 days, widespread rash starting on trunk, spreading to face, scalp and extremities

Erythematous macules –> papules –> vesicles with clear fluid on erythematous base –> eruption of vesicles –> crusted papules –> hypopigmentation of healed lesions.

+ severe pruritus, headache, myalgia, arthralgia, myalgia, fever

171
Q

How is chickenpox managed?

A

Self-limiting- not harmful

Antihistamines
Topical calamine lotion- reduces itching

172
Q

Give 3 predisposing factors for shingles

A 
Advancing age
Immunocompromised 
Chronic stress
Malnutrition 
Malignancy
173
Q

What is the pathophysiology of shingles?

A

Varicella zoster virus is reactivated and replicated in the dorsal root ganglia and travels on the peripheral sensory nerves to the skin.

174
Q

What are the clinical features of shingles?

A

Fever
Headache
Fatigue
Paresthesia
Itching
Severe pain –> burning, throbbing, stabbing
Rash –> erythematous maculopapular rash that becomes vascular lesions distributed in a dermatomal pattern

175
Q

What is Herpes Zoster Ophthalmicus?

A

Reactivation of herpes zoster in the ophthalmic branch of the trigeminal nerve

Reduced corneal sensitivity with severe pain in forehead and bridge of nose.

176
Q

What is Herpes Zoster Ophthalmicus?

A

Reactivation of herpes zoster in the geniculate ganglion affecting the 7th and 8th cranial nerve.

Facial nerve paralysis (Ramsay Hunt Syndrome), vertigo, sensorineural hearing loss

177
Q

How is shingles managed?

A

Anti-inflammatories
Analgesia
Aciclovir

178
Q

Give 3 predisposing factors for a tinea infection

A

Diabetes
Immunodeficiency
Poor circulation
Sweaty/wet skin

179
Q

What is tinea pedis?

A

Fungal infection of the foot

Chronic pruritic erythematous scaling and erosions between the toes
Hyperkeratotic thickening of the soles of the feet
Pruritic and painful lesions on the medial foot

180
Q

What is tinea capitis?

A

Fungal infection of the scalp

Round, pruritic scaly plaques with broken hair shafts/alopecia

181
Q

What is tinea unguium?

A

Fungal nail infection- discoloured brittle nail

182
Q

What is tinea cruris?

A

Fungal infection of the inguinal area.

Pruritic erythematous plaque with scrotal sparing

183
Q

What is tinea corporis?

A

Affecting a location other than feet, scalp, nails and groin.

Round pruritic plaque with central clearing and a scaling raised border

184
Q

How is tinea managed?

A

Skin- topical antifungal
Scalp- oral antifungal + ketoconazole shampoo
Nails- amorolfine paint, removal of nail if severe

185
Q

Give 2 risk factors for a candida albicans infection

A

Immunosuppression

Imbalance in local flora- antibiotics, steroids, pregnancy, AML, myeloma, smoking

186
Q

Describe the clinical features of a candida albicans infection

A

Erythematous patches and satellite lesions

Found in skin folds and between digits

187
Q

How is candida albicans infection managed?

A

Topical antifungal

188
Q

Give 3 predisposing factors for a pityriasis versicolor infection

A 
15-24 years old
Tropical climate
Excessive sweating 
Cushing's 
Immunosuppression
189
Q

What are the clinical features of pityriasis versicolor?

A

Round, well-demarcated macules that reveal a fine subtle scale
Areas of hypo and hyperpigmentation
Do not tan in sunlight
Mild pruritus

190
Q

What is the pathophysiology of pityriasis versicolor?

A

Fungal infection of the stratum corneum which degrades lipids. This produces acids which damage melanocytes and cause inflammation.

4. Senior Block- Special Senses (4 decks)

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