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4. Senior Block- Special Senses > Dermatology > Flashcards

Dermatology Flashcards

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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
What is lichenification?
Thickening of the epidermis with exaggerated skin markings and scratching
26
What is purpura?
Blood in the skin- non-blanching
27
What is erythema?
Red skin due to local vasodilation
28
What are striae?
Stretch marks
29
Give 3 risk factors for benign melanocytic naevi
Family history Sunburn Excess sun exposure Fair skin
30
What is the pathophysiology of the development of benign melanocytic naevi?
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
31
How are benign melanocytic naevi managed?
No need to remove Wear suncream Watch for mole changes Can remove for cosmetic reasons or trauma or suspicion of melanoma
32
What is a seborrhoeic keratosis?
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
33
What is the management of seborrhoeic keratoses?
Leave them alone Cryotherapy Curettage removal + biopsy
34
What is an epidermal cyst?
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
35
Who do epidermal cysts affect?
Young to middle age adults | Common in acne
36
How are epidermal cysts managed?
Leave alone Can surgically remove Antibiotics if infected
37
What is a pilar cyst?
Cyst full of keratin but lining made up of cells found at the root of hairs. Commonly found on the scalp.
38
What is a dermatofibroma?
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.
39
How is a dermatofibroma managed?
Spontaneous resolution Removal under LA Cryotherapy Intralesional steroid injections
40
Describe a cutaneous neurofibroma
Circumscribed superficial soft brown/skin coloured nodules with buttonhole invagination.
41
Describe a subcutaneous neurofibroma?
Circumscribed soft brown/skin coloured nodules with buttonhole invagination. Deep in the skin so causes tenderness
42
What is a plexiform neurofibroma?
Bag-like mass found within the skin. Invasive tumours which involves all layers of the skin, muscle, bone and blood vessels.
43
What is a cafe au lait patch and what condition do they suggest?
Well-defined, oval, light brown patches >0.5cm Neurofibromatosis if >5 patches
44
What is a keratoacanthoma?
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
45
How is a keratoacanthoma managed?
Look very similar to SCC! So excise and biopsy
46
What is a strawberry naevus?
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.
47
Give 4 risk factors for strawberry naevus development
Low birth weight Prematurity Multiple gestation Chorionic villus sampling
48
How is a strawberry naevus managed?
Do nothing Topical beta blocker Surgical excision --> very vascular structure so be very careful
49
What is a pyogenic granuloma?
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
50
How is a pyogenic granuloma managed?
Cryotherapy Curettage Creams --> topical timolol and steroids
51
Give 3 risk factors for actinic (solar) keratoses
Excess sunbathing Sunbed use Outdoor work Type 1 skin
52
What is the pathophysiology of actinic (solar) keratoses
Sun induced dysplastic intra-epidermal proliferation of atypical keratinocytes. Skin becomes thicker
53
What are the clinical features of actinic (solar) keratoses?
Crumbly, yellow, scaly, crusty lesions Rough feeling Surrounding skin- blotchy, freckled, wrinkled Sun exposed areas
54
How are actinic (solar) keratoses managed?
``` Sun protection Cryotherapy Surgical removal under LA Creams --> 5-fluorouracil, diclofenac, Imiquimod Photodynamic therapy ``` *Need treating as can turn into SCC*
55
What is Bowen's disease?
Squamous cell carcinoma in situ
56
Give 4 risk factors for Bowen's disease
Long term sun exposure Immunosuppression Post radiotherapy HPV infection on genitals
57
What are the clinical features of Bowen's disease?
Slowly enlarging red, scaly plaque with flat edge | Found on sun exposed skin
58
How is Bowen's disease managed?
*5% progress to SCC* ``` Cryotherapy Curettage Excision Creams --> 5-fluorouracil, Imiquimod Photodynamic therapy Radiotherapy ```
59
Give 4 pieces of advice you could give to a patient about avoiding sun damage to the skin
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
60
Give 4 predisposing factors for basal cell carcinoma
``` Sun exposure Immunosuppression Tanning beds Type 1 skin Radiotherapy Previous BCC FHx of BCC ```
61
What is the pathophysiology of basal cell carcinoma?
Cancer of the basal cells in the epithelium. Highly localised and does not spread but can invade local tissue
62
Describe a typical basal cell carcinoma lesion
``` Nodule with raised pearly edges Central ulceration Visible surface telangiectasia May bleed, crust over, ooze Will not heal Found on sun exposed areas ```
63
How is a basal cell carcinoma managed?
Wide excision Curettage and electrodesiccation Mohs surgery --> microscopy done at time of surgery Radiotherapy Photodynamic therapy --> very early cancer
64
Give 4 risk factors for squamous cell carcinoma
``` sun exposure Immunosuppression HPV infection Type 1 skin Albinism History of sunburn Actinic keratoses Xeroderma pigmentosum ```
65
What is the pathophysiology of squamous cell carcinoma?
UV light causes mutations in the DNA of keratinocytes in the epidermis resulting in cancerous changes
66
Give 4 clinical features of squamous cell carcinoma
Scaly nodule with red inflamed base Presistanty ulcerated Sore, tender, bleeds Found on sun exposed areas
67
How is squamous cell carcinoma managed?
Excision | Mohs surgery
68
Where do squamous cell carcinomas tend to metastasise to?
Lymph nodes | Surrounding tissues
69
Give 4 risk factors for malignant melanoma
``` Sun exposure Sun burn FHx of MM Advanced age Immunosuppression Type 1 skin >50 benign melanocytic naevi Previous melanoma Sunbed use ```
70
What are the 4 types of malignant melanoma?
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%)
71
What is the A-F of assessing potential melanomas?
``` Asymmetry Borders (irregular, poorly defined) Colour variation Diameter (>7mm) Evolution Funny looking --> mole looks different to others around it ```
72
What is the Breslow score in melanoma management?
Measurement of how far melanoma cells have spread down from the surface in mm
73
How are malignant melanomas staged?
Using TNM (with help of Breslow for T score) TNM translated to Stage 0-4
74
Briefly describe stages 0-4 of malignant melanoma
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
75
How are malignant melanomas managed?
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)
76
Give 4 common sites for malignant melanoma to spread to
``` Lungs Liver Bone Brain Abdomen Lymph nodes ```
77
Where are melanomas most commonly found on men and women?
Men: back Women: shins
78
What is anaphylaxis?
Severe and life-threatening reaction to a trigger such as nuts, drugs, insect stings, GA, latex, milk.
79
How does anaphylaxis manifest in the skin?
Pruritus Erythema Urticaria Angioedema
80
What is angioedema?
Swelling of the deep dermis usually in the hands, feet, orbits, lips, tongue and genitals
81
How is anaphylaxis managed?
Remove trigger Use Epipen Recovery position A-E resuscitation
82
What is erythroderma?
Intense and widespread erythema due to inflammatory skin disease
83
Give 4 causes of erythroderma
``` Idiopathic Psoriasis Atopic dermatitis Cutaneous T cell lymphoma HIV infection Drug eruption (Sulphonamides, Alopurinol, Carbamazepine, Gold) ```
84
Give 4 systemic complications of erythroderma
Widespread vasodilation causes erythema Heat loss, Fluid loss, Electrolyte imbalance, Skin infections, Hypoalbuminaemia
85
How is erythroderma managed?
Correct systemic problems Treat underlying cause Bed rest
86
What is necrotising fasciitis?
Rapidly progressive skin infection caused by Group A streptococcus and S.aureus.
87
Describe a necrotising fasciitis lesion
Painful, cyanotic, blistered, necrotic, deep gangrene
88
How is necrotising fasciitis managed?
Emergency! IV Abx Fluids Surgical debridement immediately
89
What is Toxic Epidermal Necrolysis (TEN)? Give 3 drug causes
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
Give 3 clinical features of TEN
Flu like symptoms Widespread painful erythema Necrosis of large sheets of epidermis
91
How is TEN managed?
``` ICU Pain relief Fluids IV immunoglobulins Protect skin ```
92
What is Stevens-Johnson Syndrome?
Severe erythema multiforme with widespread skin involvement
93
Give 2 clinical features of Stevens-Johnson Syndrome
Painful erythematous macules which become target lesions (central necrosis with ring of erythema) Mucosal ulceration
94
Give 4 drug causes of Stevens-Johnson Syndrome
Sulphonamides Anti-epileptics Penicillins NSAIDs
95
Give 4 predisposing factors for Eczema Herpeticum
``` Inflammatory skin condition Severe eczema Eczema from infancy Skin trauma Cosmetic procedures (lasers, skin peels) ```
96
What is the pathophysiology of Eczema Herpeticum?
Herpes simplex virus type 1 infects large areas of skin (often spread from a small cold sore)
97
Describe the lesions seen in Eczema Herpeticum
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
How is Eczema Herpeticum managed?
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
Describe a DIC rash
``` Petechiae Purpura Ecchymosis Blood oozes from wounds/lines Purpura fulminans- extensive skin necrosis ```
100
Give 5 potential triggers for Atopic eczema
``` Soaps Shampoos Allergens --> dust, fur, pollen Environment --> cold/dry weather, damp Wool or synthetic fabrics Skin infections Hormonal changes Stress ```
101
What are the clinical features of atopic eczema?
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
How is atopic eczema managed?
``` 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
Give 3 examples of secondary viral infections from atopic eczema
Molluscum contagiosum Viral warts Eczema herpeticum
104
What is contact dermatitis?
Eczema triggered by contact with an irritant. Reaction will occur within a few hours of contact and usually affects the hands and face.
105
What are the clinical features of discoid eczema?
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
What is the pathophysiology of venous eczema?
Valves are incompetent so venous drainage is reduced. Increased pressure in leg veins leads to damage to overlying skin which triggers inflammation.
107
Give 4 risk factors of venous eczema
``` Obesity Immobility Leg swelling Varicose veins Hx of DVT Hx of cellulitis ```
108
What are the clinical features of venous eczema?
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
What is the management of venous eczema?
``` Weight loss Raise feet up Be more mobile Avoid trauma to legs Bandaging and compression stockings Topical emollients ```
110
What is the pathophysiology of psoriasis?
Hyperproliferation of keratinocytes in the epidermis leading to proliferation and dilation of blood vessels in the dermis and an infiltration of inflammatory cells.
111
Give 5 potential triggers of psoriasis
``` Stress Skin infections Skin trauma Drugs (lithium, NSAIDs, Beta blockers, antimalarials) Alcohol Smoking Obesity Climate ```
112
Describe how chronic plaque psoriasis presents
Symmetrical well-defined red plaques with silvery scale on extensor aspects of the elbows, knees, scalp and sacrum
113
Describe how flexural psoriasis presents
Plaques in moist flexural areas eg. axilla, groin and submammary area. Symmetrical distribution. Less scaly
114
Describe how guttate psoriasis presents
Large numbers of small plaques <1cm over the trunks and limbs. Seen in young patients after a streptococcal infections. Lasts 3-4 months
115
Describe how pustular psoriasis presents
Yellow brown pustules within plaques on the palms and soles
116
Describe how generalised psoriasis presents
Entire body covered in erythematous or pustular plaques with systemic upset. Can be triggered by rapid removal of steroids
117
Describe the nail changes which occur in psoriasis
Pitting Onycholysis Thickening Subungual hyperkeratosis
118
What joint condition can also present with symptoms of psoriasis?
Psoriatic arthritis | Seronegative
119
How is psoriasis managed?
Conservative- weight loss, stop smoking, education Topical- corticosteroid, vitamin D analogue Phototherapy Oral- methotrexate, ciclosporin, acitretin Biological therapies- Infliximab, Adalimumab, Etanercept
120
What is the pathophysiology of acne vulgaris?
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
What are the clinical features of acne vulgaris?
``` Open (blackhead) and closed (whitehead) comedones Papules Pustules Nodules Cysts Commonly on face, chest and back ```
122
How is mild acne managed?
Topical benzoyl peroxide Topical retinoid Topical antibiotics
123
How is moderate acne managed?
Topical benzoyl peroxide + Topical antibiotics Oral antibiotics COCP for girls
124
How is severe acne managed?
Isotretinoin
125
Give 4 side effects of isotretinoin
``` Teratogenic - girls need monthly pregnancy tests Increased cholesterol Deranged LFTs Dry eyes, mouth, skin Depression Muscle pains ```
126
Give 3 predisposing factors for cellulitis?
Immunosuppression Open wound Leg ulcers/oedema Minor skin injury
127
What is cellulitis?
Rapidly spreading local infection of the deep dermis and subcutaneous tissue. Caused by S. aureus and Group A Streptococcus
128
What is erysipelas?
Superficial skin infection of dermis and upper subcutaneous tissue. Caused by Group A streptococcus
129
Describe how cellulitis will present
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
How is cellulitis managed?
Bed rest Analgesia Penicillin based antibiotics (Flucloxacillin, Benzylpenicillin) oral/IV Surgical debridement
131
What is an emergency complication of cellulitis?
Necrotising fasciitis
132
What is folliculitis?
Localised inflammation of a hair follicle
133
Give 3 infectious causes of folliculitis
S. aureus P. aeruginosa Candida albicans
134
Give 3 non-infectious causes of folliculitis
Ingrown hair, friction, follicular trauma, occlusion
135
How does folliculitis present?
Tender papules or pustules at the site of hair follicles
136
How is folliculitis managed?
Hygiene measures Antibacterial soap Warm compress Topical mupirocin
137
What are furuncles and carbuncles?
``` Furuncle= deep folliculitis with abscess in subcutaneous tissue Carbuncle= confluent folliculitis, abscess and skin necrosis ```
138
Give 5 predisposing factors for Impetigo infection
``` 2-6 years old Developing country Underprivileged background Warm and humid climate Atopic dermatitis Diabetes Immunocompromised ```
139
What pathogen causes bullous impetigo?
S. aureus
140
What pathogen causes non-bullous impetigo?
S. aureus or Group A streptococci
141
How does non-bullous impetigo present?
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
How does bullous impetigo present?
Vesicles grow to form large, flaccid bullae which rupture and form thin brown crusts Sloughing of the skin, trunk and upper extremities
143
How is impetigo managed?
Antibacterial washes- chlorhexidine Non-bullous= topical Abx- mupirocin, retapamulin Bullous= cephalexin Need antibiotics for 24hrs before returning to school
144
Describe the skin presentations of primary, secondary and tertiary syphilis
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
What is the pathophysiology of staphylococcal scalded skin syndrome?
Staph aureus infection produces exfoliative toxins which cleave the granular level of the epidermis, causing sheets of skin to slough off
146
How does staphylococcal scalded skin syndrome present?
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
How is staphylococcal scalded skin syndrome managed?
IV Abx= penicillinase resistant penicillin eg. nafcillin Analgesia Fluids Emollients
148
What are the two genotypes of herpes simplex virus?
Herpes simplex type 1 | Herpes simplex type 2
149
What is the pathophysiology of herpes simplex virus?
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
How does labial herpes simplex present?
24hrs before= pain, tingling, burning Recurring, erythematous vesicles which turn into painful ulcerations on the oral mucosa and lip borders
151
How does genital herpes present?
Mostly asymptomatic Rednes, swelling, tingling, pain and pruritus on genitals. Painful lymphadenopathy. Unusual vaginal discharge
152
How is herpes simplex treated?
Labial- self limiting | Genital- oral acyclovir for 7 days, hygiene measures, abstain from sex until lesions clear
153
What is erythema multiforme?
Rare, acute hypersensitivity reaction triggered commonly by a herpes simplex infection. Other triggers= fungal infections, NSAIDs, penicillins, barbiturates, immunisations
154
How does erythema multiforme present?
Target lesions (symmetrical- hands, feet) Fever Myalgia Arthralgia
155
How is erythema multiforme managed?
``` Self limiting in 1 month Stop drug cause Analgesia Antihistamines Topical steroids ```
156
Give 2 risk factors for HPV infection
Damaged skin/mucous membranes Immunodeficiency Genital HPV= unprotected sex, high number of sexual partners, early first sexual encounter
157
Describe the appearance and associated symptoms of anogenital warts
Exophytic, cauliflower-like lesions that cause pruritus, tenderness and bleeding Found on anus, penis, vulva, urethra and cervix
158
Describe the appearance and associated symptoms of common warts
Skin coloured rough scaly plaques on elbows, knees and fingers
159
Describe the appearance and associated symptoms of plantar warts
Rough hyperkeratotic lesions on sole of foot, painful when walking
160
Describe the appearance and associated symptoms of flat warts
Small flat patches or plaques on hands, face or shins
161
How are anogenital warts managed?
Cryotherapy | Local topical treatment- Fluorouracil, Imiquimod
162
How are common warts managed?
Watch and wait Cryotherapy Salicylic acid
163
How are plantar warts managed?
Wart paint | Cryotherapy
164
Give 4 predisposing factors for molluscum contagiosum
``` Male <5 years old Warm and humid climate Immunosuppression Atopic dermatitis Crowded living conditions ```
165
What do molluscum contagiosum lesions look like?
Non-tender, flesh coloured pearly dome-shaped papules with central depression 2-5mm in diameter
166
Where do children commonly experience molluscum contagiosum?
Face Trunk Popliteal fossa Antecubital fossa
167
Where do adults commonly experience molluscum contagiosum?
Lower abdomen Groin Genitalia Proximal thighs
168
How is molluscum contagiosum managed?
Spontaneous resolution in 6-9 months Cryotherapy Curettage
169
What pathogen causes chickenpox?
Varicella zoster virus
170
Describe the clinical features of chickenpox
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
How is chickenpox managed?
Self-limiting- not harmful Antihistamines Topical calamine lotion- reduces itching
172
Give 3 predisposing factors for shingles
``` Advancing age Immunocompromised Chronic stress Malnutrition Malignancy ```
173
What is the pathophysiology of shingles?
Varicella zoster virus is reactivated and replicated in the dorsal root ganglia and travels on the peripheral sensory nerves to the skin.
174
What are the clinical features of shingles?
Fever Headache Fatigue Paresthesia Itching Severe pain --> burning, throbbing, stabbing Rash --> erythematous maculopapular rash that becomes vascular lesions distributed in a dermatomal pattern
175
What is Herpes Zoster Ophthalmicus?
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
What is Herpes Zoster Ophthalmicus?
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
How is shingles managed?
Anti-inflammatories Analgesia Aciclovir
178
Give 3 predisposing factors for a tinea infection
Diabetes Immunodeficiency Poor circulation Sweaty/wet skin
179
What is tinea pedis?
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
What is tinea capitis?
Fungal infection of the scalp Round, pruritic scaly plaques with broken hair shafts/alopecia
181
What is tinea unguium?
Fungal nail infection- discoloured brittle nail
182
What is tinea cruris?
Fungal infection of the inguinal area. Pruritic erythematous plaque with scrotal sparing
183
What is tinea corporis?
Affecting a location other than feet, scalp, nails and groin. Round pruritic plaque with central clearing and a scaling raised border
184
How is tinea managed?
Skin- topical antifungal Scalp- oral antifungal + ketoconazole shampoo Nails- amorolfine paint, removal of nail if severe
185
Give 2 risk factors for a candida albicans infection
Immunosuppression | Imbalance in local flora- antibiotics, steroids, pregnancy, AML, myeloma, smoking
186
Describe the clinical features of a candida albicans infection
Erythematous patches and satellite lesions | Found in skin folds and between digits
187
How is candida albicans infection managed?
Topical antifungal
188
Give 3 predisposing factors for a pityriasis versicolor infection
``` 15-24 years old Tropical climate Excessive sweating Cushing's Immunosuppression ```
189
What are the clinical features of pityriasis versicolor?
Round, well-demarcated macules that reveal a fine subtle scale Areas of hypo and hyperpigmentation Do not tan in sunlight Mild pruritus
190
What is the pathophysiology of pityriasis versicolor?
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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