Module 7 Flashcards

1
Q

What are plane warts?

A
  • Flat topped, opaque, groups small papules
  • Often occurs at sites of trauma (Koebner phenomenon)
  • Mainly found in children - face and dorm of hands
  • Resolves spontaneously
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2
Q

What is molluscum contagiosum?

A
  • Multiple, grouped, opaque plaques with a depressed centre

- Usually occur in children

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3
Q

What is milia?

A
  • 1mm spherical papules
  • Very small, superficial infundibular cysts
  • Occur on cheek and eyelids
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4
Q

What is sebaceous gland hyperplasia?

A
  • Enlargement of sebaceous gland
  • Seen in middle-aged/older people
  • One or more umbilicated papule
  • Found on forehead and cheek
  • Yellow in colour with central depression
  • Removed using curettage, cautery or excision
  • Often mistaken for BCC
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5
Q

What is a syringoma?

A
  • Multiple small (1-5mm) flesh coloured soft papules
  • Found over lower eyelids
  • Harmless tumours of sweat glands
  • Best left alone
  • Can be removed using gentle cautery
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6
Q

What are skin tags?

A
  • Multiple pedunculate skin-coloured or brown papules
  • Found around neck/axillar
  • Snip excision or ablation with a hyrecator
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7
Q

What is trichofolliculoma?

A
  • Benign papule or nodule
  • Face or scalp
  • May be a central punctum with hair protruding from the surface
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8
Q

What is trichoepithelioma?

A
  • Skin-coloured papule or nodule
  • Face or upper trunk
  • Resembles BCC so treat as BCC unless confirmed as trichoepithelioma
  • No tx required
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9
Q

What is dermatosis papulosa nigra?

A
  • Exclusively in black population
  • Adulthood
  • Multiple 1-5mm asymptomatic, hyper pigmented papules on face and neck
  • Progresses with age
  • Benign, needing no tx
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10
Q

What is a cherry angioma?

A
  • Small 1-4mm solid, red papules
  • Appear on trunk and proximal limbs
  • > 30 years
  • Multiple lesions
  • Harmless, no tx needed
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11
Q

What is xanthelasmata?

A
  • Yellow, flat plaques usually found medial to eyelids
  • Associated with hyperlipidaemia
  • Tx with trichloroacetic acid
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12
Q

What is naevus sebaceous?

A
  • Hairless plaques
  • Congenital malformation
  • Scalp or face
  • Linear fashion, following Blaschko lines
  • Skin coloured or yellow/orange
  • Become thicker and more verrucous with age
  • Increased risk of development of BCC
  • Monitored and excised where possible
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13
Q

What is granuloma annulare?

A
  • Inflammatory condition
  • Ring of multiple dermal flesh-coloured or red papules
  • Distal extremities
  • Localised: 50% resolve spontaneously
  • Generalised: 10+ lesions at multiple sites
  • Associated with diabetes and thyroid disease
  • Tx: topical steroids, intralesional steroids, UVB or PUVA
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14
Q

What is seborrhoeic keratosis?

A
  • Benign macular or papular, velvety to verrucous lesions
  • Waxy yellow to dark brown
  • 1mm to several cms
  • Stucco keratoses: acral region
  • Common in elderly pts
  • Tx: cryotherapy, curettage and shave excision
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15
Q

What is a dermatofibroma?

A
  • Firm round nodule, small (5-10mm)
  • Skin coloured or pink/brown
  • Edge is darker
  • Dermal origin, attached to overlying skin
  • Often follows an insect bite or trauma (e.g. shaving legs)
  • Multiple dermatofibromas seen in SLE
  • Squeezing causes central lesion to dimple
  • Often left alone
  • Tx: simple excision
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16
Q

What is a pilomatricoma?

A
  • Benign tumour of hair follicle
  • Children: face and arms
  • Pink/flesh coloured nodules, 5mm-4cms
  • Some have blueish hue
  • Late lesions calcify
  • Tx: simple excision (may recur)
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17
Q

What is a lipoma?

A
  • Seen mainly on trunk
  • Solitary but multiple
  • Benign tumour of fat cells - soft, firm subcutaneous nodules
  • Multiple familial lipomatosis: autosomal dominant
  • Tx: excision
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18
Q

What is a neurofibroma?

A
  • Nerve sheath tumour seen in adults
  • Solitary, affecting trunk and head
  • Skin coloured, soft and rubbery papules or nodules
  • Asymptomatic
  • Soft with hole in base
  • If multiple, may be part of Recklinghausen’s disease (Neurofibromatosis type 1)
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19
Q

What is a leiomyoma?

A
  • Benign SM tumour or erector pili muscle
  • Group of superficial pinhead to pea-sized firm nodules
  • Back, face or extensor surface of extremities
  • Painful when cold
  • Tx: excised if symptomatic
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20
Q

What is a trichilemmal (pilar) cyst?

A
  • Firm, spherical skin-coloured nodules
  • Occur on scalp
  • Tx: removal bu enucleation
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21
Q

What is a infundibular (epidermoid) cyst?

A
  • Found on face, neck and chest
  • Small punctum
  • Often rupture leading to chronic inflammation
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22
Q

What is a dermoid cyst?

A
  • Look like infundibular cysts
  • Present from birth or early childhood
  • Head and neck (midline or lateral edge of eyebrow)
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23
Q

What is a pyogenic granuloma?

A
  • Vascular, proliferative lesion
  • Response to trauma presenting as red, ulcerated mass
  • Grow rapidly over a few weeks
  • Bleed easily when touched
  • Ddx: amelanotic melanoma
  • Tx: Refer appropriately if any doubt, curettage, cautery, sample to histology
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24
Q

What is a melanocyte?

A
  • Specialised pigment producing cells
  • 5-10% basal cells in epidermis
  • Originate in neural crest and in fetal life they migrate to the dermo-epidermal junction where they reside
  • Melanocytes are dendritic and via dendritic processes secrete melanin particles (called melanosomes) into neighbouring keratinocytes
  • Skin colour determined by number and distribution of melanosomes and their melanin content
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25
Q

What is a mole?

A
  • Benign proliferation of melanocytes -> melanocytic naevus
  • Common, multiple pigmented papules
  • Histologically nests of melanocytic naevus cells
  • Acquired and develop during childhood or adolescence
  • Reach plateau in 3rd decade
  • Rare in old age, slowly disappear
  • Inherited trait, more common in caucasian
  • Increase following sun exposure, pregnancy, immunosuppression
  • Type of mole dictated by position in dermis
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26
Q

How does location dictate type of mole?

A

Junctional:

  • At dermo-epidermal junction
  • 0.1-1cm, dark brown, evenly pigmented, symmetrical macule or even slightly elevated
  • Children - any body site
  • Adults - palm, soles, genitalia

Compound:

  • At both dermo-epidermal junction and within dermis
  • Slightly raised, can occur at any site
  • Light-brown pigmented papules to dark-brown papillomatous and sometimes hyperkeratotic

Intradermal:

  • ‘mature’ mole, all intradermal
  • Usually arise in 3rd decade
  • Skin coloured papules
  • dome-shaped, papillomatous nodules, pedunculate skin tags
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27
Q

What is congenital hairy naevus?

A
  • present at birth
  • bigger, >1cm in size, light brown to black
  • Later become protuberant and hairy
  • Bathing trunk naevus - >20cm, whole trunk or gluteal region, rare, significant lifetime risk of malignant transformation
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28
Q

What is atypical melanocytes (dysplastic) naevus?

A
  • Mole with atypical clinical and/or histological features
  • > 5mm in size, irregular border ‘smudged’ border, irregular pigmentation, erythema, papular and macular component
  • Numerous moles (often >100)
  • Unusual distribution, non sun-exposed areas (buttocks, genitalia, scalp, soles, dorsum of feet)
  • 10-fold risk of melanoma
  • autosomal dominant
  • up to 400-fold risk of melanoma where first degree relative have atypical naevi
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29
Q

What is a spitz?

A
  • discrete, reddish brown or pink
  • benign rounded nodule
  • grows rapidly on face of child (called juvenile melanoma)
  • stop growing after reaching 1-2cm in size
  • Histologically: proliferative and spindle-shaped naevus and dilated dermal blood vessels
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30
Q

What is a halo?

A
  • Trunk in children or adolescents
  • Destruction by body’s immune system of naevus cells within a naevus
  • White halo of depigmentation surround the pre-existing mole which subsequently involutes
  • ?association with vitiligo
  • Appear simultaneously
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31
Q

What is Becker’s naevus?

A
  • much larger than most melanocytes naevi
  • prescent in adolescent males
  • flat, unilateral hyperpigmented area of skin
  • upper back, chest or shoulder
  • later becomes hairy
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32
Q

What is blue naevus?

A
  • deep dermal aggregate of melanocytes
  • blue colour
  • melanocytes migrating from neural crest to epidermis during fatal life become arrested within the dermis
  • smooth solitary nodule on face of older children or hand of young adults
  • Mongolian blue spots on sacral-gluteal region of newborn babies (disappears by age of 5)
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33
Q

What is malignant melanoma?

A
  • malignant tumour of melanocyte
  • most serious form of skin cancer
  • metastasises early, no curative treatment after this
  • incidence is doubling every decade
  • increased sun exposure - intense, excessive burning-type experienced on holiday
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34
Q

What are the risk factors for malignant melanoma?

A

Sunlight:

  • intensive bursts of UV radiation in childhood
  • transformation of benign melanocytes into malignant phenotype
  • incidence higher closer to equator
  • risk greater with episodic exposure e.g. office works on holiday, than with continuous sun exposure e.g. outdoor workers

UV radiation:

  • most important environmental factor
  • in those who are constitutionally at risk

Skin colour:

  • Fitzpatrick type 1 skin (always burns, never tans)
  • Red hair and freckles
  • Large number of melanocyte naevi (>100) - correlates to sun exposure in childhood
  • Large congenital melanocytes naevi esp giant congenital naevus higher risk

Family Hx:
- FHx of melanoma + FHx atypical moles gives greatest risk

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35
Q

What are the clinicopathological variants of melanoma?

A

Superficial spreading melanoma:

  • Most common
  • Female leg, male back, young
  • Hx of slowly expanding pigmented lesion
  • Initially flat lesions (horizontal growth), while tumour thickness less than 0.75mm good prognosis
  • Later downwards vertical growth - prognosis deteriorates, increased risk of mets
  • Asymmetric lesion, irregular lateral margin, irregular multicoloured pigmentation, hx of growth
  • 1/3 arise from pre-existing mole or freckle

Nodular melanoma:

  • Worse prognosis as tumour already has vertical downwards growth
  • > males, in trunk
  • Rapidly growing black nodule (much of pigmentation is due to blood not melanin)

Lentigo maligna melanoma:

  • Arises in a long-standing lentigo maligna
  • In situ melanoma, sun exposed part of face
  • Person spent many years outdoor
  • Large irregular freckle that slowly emerges over years
  • At some point transforms into malignant melanoma (invasive nodule develops inside pre-existing lentigo maligna)

Acral lentigous melanoma:

  • More common in asians/afro carribeans
  • Non-hair bearing skin - palms, soles, nails
  • Presents late, poor prognosis
  • Nail melanoma - irregular pigmentation under or around nail (big toe/thumb), Hutchinson’s sign (abnormal pigmentation on proximal nail fold margin)

Amelanotic melanoma:

  • non-pigmented
  • delay in identifying results in poor prognosis
  • these can arise anywhere where there are melanocytes inc mucosal epithelia, retina
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36
Q

How to identify melanomas?

A

A - asymmetry
B - border irregularity
C - colour irregularity/variable pigmentation
D - diameter >7mm
E - elevation/enlargement (emerges over weeks to months)

Others: inflammation, bleeding, oozing, crusting, mild itch

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37
Q

What is the most significant and consistent prognostic factor?

A

Tumour thickness or depth of primary melanoma (a.k.a Breslow thickness)

Clark level of invasion - tumours thinner than 0.5mm almost never metastasise

Others:

  • Vertical growth phase
  • Sex (M>F)
  • Age (older age)
  • Diameter of lesion
  • Clinical ulceration
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38
Q

Survival rates of melanoma.

A
95% for up to 0.75mm
85% for 0.76 to 1.5mm
70% for 1.6 - 3mm
50% for > 3mm
40% for > 3.5mm
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39
Q

What is the recommended treatment for melanoma?

A
Excision margins: 
In situ - 0.5cm 
<1mm thick - 1cm 
1-4mm thick - 1-2cm 
>4mm thick - 2-5cm 

Melanoma in situ and lentigo maligna have no metastatic potential so excise with margin of 0.5cm

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40
Q

How does melanoma spread?

A

Lymphatic drainage system

41
Q

How do you stage patients with intermediate thickness melanoma (1-4mm)?

A

Sentinel lymph node biopsy

42
Q

What are the pre-cancerous lesions that can evolve into a SCC?

A

Actinic keratosis

SCC in-situ (Bowen’s disease, Erythroplasia of Queryat)

43
Q

What is the median age of onset of SCC and BCC?

A

SCC - mid 70s

BCC - late 60s

44
Q

What are the risk factors for NMSC?

A

Sunlight:

  • SCC - chronic sun exposure and acute episodes of sunlight
  • BCC - acute sunburn, especially in childhood

PUVA (photochemotherapy)

Arsenic:

  • present in well water and medicinal potions
  • typical lesions palmoplantar keratoses

HPV: - SCC development, anogenital and periungal regions

Smoking: - oral SCC

Poor oral hygiene: - oral SCC

Genetic syndromes:

  • Xeroderma pigmentosum - autosomal recessive disorders of defective DNA repair, freckling and sun sensitivity in childhood, strict sun avoidance needed
  • Oculocutaneous albinism - esp SCC
  • Gorlin’s syndrome - rare, autosomal dominant condition, multiple BCCs, palmar pits, jaw bone cysts, skeletal abnormalities

Chronic wounds: - SCC

Immunosuppression:

  • organ transplant recipients at greater risk
  • SCC
45
Q

What is actinic keratosis?

A
  • Pre-malignant lesion
  • Poorly circumscribed erythematous macules and papules
  • Chronic UVA exposure
  • Face, ears, dorsum of hands and bald scalps
  • Solar keratoses have scale
  • 4th and 5th decade, pale skinned, sun damaged skin
  • Pink, red, brown scaly patches or plaques
  • mm to cm in size
  • Can become thick plaque or cutaneous horn, rough on palpation
  • Actinic chelitis involves the lips
  • Potentially transform into SCC
  • Tx: 5-fluorouracil or topical diclofenac, topical imiquimod increasingly being used, surgical involved cryotherapy, curettage, formal excision, PDT
46
Q

What is SCC in situ?

A
  • Full thickness intra-epidermal SCC
  • Bowen’s disease - solitary red plaque, sharp border sun exposed areas, common on lower legs
  • Erythroplasia of Queyrat - affects male genitalia, shiny red plaque, common in uncircumcised men
  • Both rarely progress to invasive SCC
  • Tx: 5-fluorouracil or topical diclofenac, topical imiquimod increasingly being used, surgical involved cryotherapy, curettage, formal excision, PDT
47
Q

What are the different types of BCC?

A

Nodular:

  • Most common type
  • Head and neck
  • > 60
  • Pearly pink papule or nodule, overlying telangiectasia, centre sunken, crusted or ulcerated

Superficial:

  • Chest or upper back
  • Younger patients with sun damage
  • Well-defined pink plaque with pearly border

Morphoeic:

  • Rare
  • Head and neck, older patients
  • Indurated plaque, appears like scar, margins difficult to visualise
48
Q

How do you diagnose BCC?

A

Punch biopsy
Incision
Excision

49
Q

How are BCCs managed?

A

Excision: allow 4mm margin

Curettage and cautery: not in recurrent or high risk BCC (e.g. around nose and eyes)

Mohs’ microscopic surgery: For BCC on nose, nasolabial folds, eyes, ears, lips. Especially if morphoeic >2cm

Radiotherapy: older patients, not easily resectable tumours

Medical therapy: 5-fluorouracil, multiple superficial BCCs on trunks and lower limb

Photodynamic phototherapy: application of photosensitising chemical and subsequent exposure to light, small BCCs at low risk site

50
Q

What factors affect prognosis of BCC?

A

High risk sites - nose, nasolabial folds, lips, ears, arounds eyes

Large tumours >2cm diameter

Recurrent tumours

Histologically, micro nodular or infiltrative tumours

51
Q

What are the clinical features of SCC?

A
  • Sun exposed sites - head, neck, arms
  • SCCs in non-sun exposed skin behave more aggressively
  • Pink, red or skin coloured plaques or nodules
  • Surface may be smooth, keratotic, crusted or ulcerated
  • May bleed easily + pain
52
Q

How is an SCC diagnosed?

A

Incisional or punch biopsy

53
Q

What factors affect the metastatic potential of SCC?

A

High risk sites:
- Lip, ear, non-sunexposed sites, arising from chronic wound

Diameter:
- Tumours >2cm in diameter 3x as likely to metastasise

Depth:
- Tumours extending in SC tissue are more likely to recur and metastasise

Histological:
- Poorly differentiated tumours + those with perineurial involvement are more likely to metastasise

Host immunosuppression

54
Q

How are SCCs managed?

A
  • Excision with 4mm margin
  • High risk require Mohs’ micrographic surgery
  • Radiotherapy - non-resectable tumours
  • Regular follow up for 5 years
55
Q

What is sclerotherapy?

A

The targeted elimination of small vessels, varicose veins and vascular malformations by the injection of a sclerosant into the lumen of the vessel

Aims to damage the vessel wall and transform it into a fibrous cord that cannot be recanalised

56
Q

What are the indications for sclerotherapy Tx:

A
  • Varicose veins
  • Low-flow vascular malformations
  • Symptomatic hemangiomas
  • Benign vascular tumours
  • Telangiectasia or spider veins
  • Reticular veins
57
Q

Describe LL venous anatomy.

A

Deep veins: femoral, popliteal, anterior + posterior tibial, peroneal

Superficial veins: great saphenous (medial), short saphenous (lateral), subdermal lateral venous system

Perforators connecting deep and superficial system

58
Q

What is the pathophysiology of lower limb venous insufficiency?

A

Haemodynamic factors:

  • Prolonged gravitational hydrostatic pressure causes retrograde failure of venous valves leading to venous hypertension and varicose veins
  • Valve incompetence in deep or superficial veins
  • Allows backwards transmission of the pressure gradient from deep to superficial system
  • Occurs through saphenofemoral junction and perforating arteries

Vein wall factors:

  • Intimal and smooth muscle cell hyperplasia
  • Luminal diameter is larger than normal
  • Skip lesions (alternate areas of thickened/fibrotic walls with thin/collapsed areas)

Potential causes of increased deep venous pressure:

  • obesity, pelvic masses
  • AV malformations
  • multiparity
59
Q

What are varicose veins?

A

Ectatic, tortuous, dilated veins that are often associated with incompetent valves

At least 3mm in size

Increased risk of superficial vein thrombosis

60
Q

What are telangiectasia?

A

Flat, red vessels smaller than 1mm in diameter

61
Q

What are venules?

A

Blue, between 1-2mm

62
Q

What are reticular veins?

A

2-4mm in diameter

63
Q

How do you classify chronic venous disorders?

A

C - clinical manifestations
E - etiological factors
A - anatomic distribution
P - underlying pathophysiology

64
Q

What are the different sclerosing agents?

A

Detergents: disrupt vein cellular structure

  • sodium tetradecyl sulfate (fibrovein)
  • polidocanol (aethoxysclerol, sclerovein)
  • sodium morrhuate - scleromate
  • ethanolamine oleate - ethamolin, neosclerol

Osmotic agents: causes damage by shifting the water balance through cellular osmotic dehydration and cell membrane denaturation

  • hypertonic saline solution
  • sodium chloride + dextrose

Chemical irritant: damage the cells wall

  • chromated glycerin - scleremo
  • polyiodinated iodine - sclerodine
  • alcoholic solution of zein - ethibloc
  • OK 432 - picibanil
  • bleomycin
65
Q

How do you manage chronic venous in sufficiency?

A

Microsclerotherapy
- telangiectasia, reticular veins

Sclerotherapy

  • varicose veins, spider veins/telangiectasia, reticular veins
  • second line after endovenous ablations

Laser and intense-pulse light therapy

Radio-frequency or laser ablation

Ambulatory phlebectomy

Surgical approaches:

  • ligation of saphenophemoral junction with vein stripping
  • phlebectomy performed through micro incisions
  • endovenous RF thermal ablation
  • endogenous laser thermal ablation
66
Q

What aspects of history should you ascertain before deciding on microsclerotherapy/sclerotherapy?

A

PMHx:
Raynauds, vascular insufficiency, DM, HTN, IHD

Social Hx:
Smoking, physical activity, occupation

Family Hx:
Venous insufficiency

Pregnancy

Drug Hx:
Oestrogen, HRT, oral contraceptives, aspirin, NSAIDS

Hx of previous episodes

67
Q

What are the symptoms of varicose veins?

A
Leg heaviness
Exercise intolerance
Pruritis
Pain and tenderness across the course of a vein 
Burning sensation 
Restless legs
Night cramps
Oedema
Skin changes
Paraesthesia
68
Q

What are symptoms of telangiectasia?

A
Burning
Cramping
Swelling 
Throbbing
Leg fatigue
69
Q

What should you look for on clinical examination of LL?

A
  • Skin changes - evidence of stasis e.g. ulceration, dermatitis
  • Prominent varicose veins, telangiectasias, small vessels, large vessels
  • DVT
  • Palpate for firm, thickened and thromboses superficial veins
  • Arterial pulses
  • Pulsations or bruits
  • Scars
  • Previous sclerosant injections
70
Q

What investigations would you request for patients with chronic venous insufficiency?

A

Duplex Ultrasonography

  • location and patency of perforators
  • flow of lesion in AV malformations

CT scan/MRI

  • venous imaging
  • assess extent and depth of malformation

Physiologic tests

  • Venous refiling time
  • Maximum venous outflow
  • Calf muscle pump EF

Other Ix: FBC, clotting studies, BM, ECG

71
Q

What is the procedure for microsclerotherapy?

A
  1. Perform duplex US to evaluate for GSV reflux - if larger than telangiectasia and small reticular veins
    - in case of reflux, GSV should be closed by other means including laser or radio-frequency ablation, adhesive agents, US-guided foam sclerotherapy
  2. Prepare - proper lighting, comfortable positioning, adequate exposure, clean with sterile technique, dilute sclerosant if needed
  3. Foam generated in 1:4 sclerosant to air ratio
  4. Inject proximally to distal starting with larger reticular veins
    - solution can be seen to infuse from reticular veins to smaller distal telangiectasia
    - quantity injected should fill vessel uniformly
    - when intravascular blood is displaced, vein should no longer be seen
    - max amount of foam used in one session is ?30mls
72
Q

What are the advantages of foam sclerotherapy?

A

Minimally invasive and therefore fewer side effects
Easily repeatable
Low cost

73
Q

What is post-procedure care for sclerotherapy?

A

Compression stockings worn immediately after procedure for 7 days, 24 hrs a day

  • more effective endosclerosis due to apposition of vessel wall
  • limits thrombus formation
  • decreases post treatment pigmentation

Mild exercise like walking for 30 mins a day

Avoid hot baths and sun exposure

Healing may take several weeks - veins initially look worse due to inflammatory changes

Follow up at 2 weeks, use 22G needle to drain any coagulum

Re-treatment can be done at 6-8 weeks

74
Q

What is dermabrasion?

A

The removal of a proportion of the dermis by abrasion

75
Q

What are the different types of dermabrasion?

A
  • Mechanical
  • Manual
  • Microdermabrasion
  • Crystal
  • Crystal free
76
Q

What are the approaches to scar revision?

A
  1. Excision - shave, elliptical, intralesional, serial
  2. Lengthening/re-orientation - Z-plasty, W-plasty, geometric broken-line closure
  3. Acne/atrophic scar revision - subcision, punch excision, punch elevation, punch grafting
  4. Fillers - injectables, fat grafts, dermal grafts
  5. Dermabrasion
77
Q

Describe mechanical dermabrasion.

A
  • Rotating abrading drums held within a drill chuck even out surface irregularities over a field of acne scarring
  • Between highest and deepest scarring
  • Need some dermis and adnexal remnants to ensure no worsening/new scarring
  • Some tx with retinoic acid and hydroquinone 4% for month preaching procedure, encourages re-epithelialisation and avoid post-inflammatory hyperpigmentation
  • Less subtle and controllable than CO2 laser resurfacing
78
Q

Describe manual dermabrasion.

A
  • Sterilised sandpaper

- Simpler and cheaper

79
Q

Describe microdermabrasion.

A
  • Inert abrasive crystals (aluminum oxide) are projected into skin and then sucked away by vacuum in a closed system
  • Acne scarring, melasma, facial rejuvenation
  • Somewhere between superficial peel and CO2 resurfacing
  • Depth of dermabrasion: vacuum pressure, particle size, angle of impaction, number of passes, probe speed
80
Q

Define microneedling.

A

The process by which micro-injuries are inflicted to the skin in a controlled fashion, triggering new collagen synthesis, without the risk of permanent scar.

81
Q

Describe collagen induction therapy.

A
  • percutaneous collagen induction creates numerous micro clefts through the epidermis into the papillary dermis
  • creates confluent zone of superficial bleeding that stimulate normal wound healing
  • non-ablative so low risk of hyperpigmentation
82
Q

What is cicatrisation?

A

Contraction of fibrous tissue at wound site by fibroblasts, leading to smaller scar but distorted tissue

83
Q

Describe normal stimulation of collagen production.

A

Platelets and neutrophils release GFs that enhance IC matrix production, such as:

  • TGF B
  • platelet derived GF
  • CT activating protein III
  • CT GF

Monocytes produce GF to increase production of:

  • Collagen III
  • Elastin
  • GAGs

5 days after injury, a fibronectin matrix forms with an alignment of fibroblasts that determines the deposition of collagen

Collagen III converted to collagen I (lifetime of 5-7 days)

Collagen tightens naturally over next few months

84
Q

What is a skin needling rolling device?

A
Micro-needling device 
Needle length varies from 0.13mm to 3mm 
0.13mm and 0.2mm - cosmetic type
Create micro channels on stratum corneum
Transdermal delivery of lipopeptides and anti-ageing products 

Lengths of 0.5mm - medical rollers
Create micro channels through epidermis into papillary dermis
Single use

85
Q

What are the indications for micro-needling?

A

Wrinkles

Scars:

  • Acne scars - more useful in boxscars, not useful for icepick scars
  • Post-burn scars

Striar distensae

Mesotherapy - micro needling enhances transdermal delivery of hydrophilic macromolecules

Hyperpigmentation/Melasma

Cellulite

Lax skin

Treatment of alopecia?? under Ix

86
Q

What are the contraindications for micro-needling?

A
  • Active acne, herpes labialis
  • Chronic skin disease (eczema, scleroderma, psoriasis, keloid scars)
  • Bloods clotting disorders, anticoagulants
  • Rosacea
  • Skin malignancy
  • Aspirin (should stop for 3 days before tx)
  • Active skin infection
  • Immunosuppression
87
Q

What is the method for micro-needling?

A
  • Skin is prepared for 1 month before Tx with topical vitamin A and vitamin C (maximises dermal collagen formation)
  • Topical anaesthetic to prepare area 45 mins before Tx
  • Performed with dermaroller with pressure in vertical, horizontal and diagonal directions 15 to 20 times. For those with deeper scars, skin is stretched so that base of scar is reached.
  • Endpoint is point-point bleeding
  • Area wiped with saline-soaked gauze to absorb blood and serous ooze
  • Topical product applied at this point e.g. vitamin A and vitamin C
  • Topical Abx cream can be prescribed
88
Q

What is after care for micro-needling?

A

Erythema seen for 2-3 days

Photoprotection is advised for weeks after Tx
Continue topical Vitamin A and C (maximise initial release of GF and stimulate collagen)

Tx can be repeated after 6 weeks
3-4 Tx are needed

89
Q

What are the disadvantages of micro-needling?

A

Need for complete anaesthesia to skin

Swelling and bruising seen in first few days

Final results take longer than laser resurfacing - however effect is longer lasting

Side effects: pain, reactivation of herpes, impetigo, allergic contact dermatitis, exposure to blood

90
Q

What are the effects of using Vitamin A and C during micro-needling?

A

Vitamin A:

  • essential for skin
  • expresses influence on 400 to 1000 genes that control proliferation and differentiation of all major cells in epidermis and dermis
  • Implied in controlled release of TGF B3 - favours development of regenerative lattice-patterned collagen network

Vitamin C:
- production of normal collagen

PCI and vitamin A regulate fibroblasts to produce collagen and therefore increase need for vitamin C

91
Q

How can radio-frequency be combined with other aesthetic methods?

A

Radiofrequency increases fibroblast proliferation to increase dermal thickening –> increases longevity of other cosmetic aesthetic techniques

  • optimal results with peels, intradermal injection of DNA nucleotides, HA injections, cosmeceuticals
  • increased pro-collagen formation
92
Q

How can botulinum toxin and fillers be combined?

A

Neurotoxins treat dynamic wrinkles
Fillers help to restore facial volume

  • longer lasting effects of filler when underlying muscle is chemo-denervated
  • less dissipation of hyaluronic acid implant as less movement
  • can be combined in same needle
93
Q

How can acetyl-hexapeptide-3 and botox be combined?

A

Acetyl-hexapeptide-3 inhibits repetitive muscular contraction similar to botox preventing formation of and stability of SNARE complexes thereby inhibiting catecholamine exocytosis
Dualistic use of topical and IM agent

  • Can be given combined or topically alone for those who don’t want invasive Tx
  • Low side effect profile
94
Q

How can micro needling and cosmeceuticals be combined?

A

Microneedling creates micro holes through SC, epidermis and dermis (depending on length) allowing penetration of cosmeceuticals into the skin

95
Q

How can microdermabrasion and cosmeceuticals be combined?

A

Microdermabrasion enhances transdermal delivery of cosmeceuticals through the partial removal of SC and increase skin permeability

  • increased delivery of nicotinamide (hydrophilic)
  • not increase retinol (lipophilic)
96
Q

How can US and cosmeceuticals be combined?

A

Low frequency US shown to increase permeability of skin to topical agents - transient cavitation
(Low frequency sonophoresis)

  • improved acne scarring
  • direct mechanical impact of gas bubbles collapsing on the skin surface results in micro jets and shock waves
97
Q

How can lasers and cosmeceuticals be combined?

A

Fractional laser creates vertical columns of thermally-ablated tissue which can be used to bypass the SC into the epidermis and dermis

  • enhance healing, reduce side effects, extend duration of benefits
  • Vit A - before procedure improve wound healing, increase collagen neo-genesis, activate fibroblasts to enhance re-epithelialisation
  • Vit C - photo-protective, anti-inflammatory, promotoes collagen neo-genesis, improved fine lines and wrinkles
  • Vit E - antioxidant, free radical scavenger, reduce erythema, scar formation, improve dyspigmentation
  • Vit K - bruising and purpura (co-factor for clotting factors)
  • GF - wound healing
  • Skin lightening agents - post-treatment hyperpigmentation
  • Moisturisers - promotes re-epithelialisation by direct delivery
98
Q

How can surgery, lasers and filler be combined?

A

Surgical correction through tightening can achieve what a minimally invasive technique cannot.

  • Large cutaneous flap rhytidectomy and SMAS plication plus HA injection on nasolabial folds and lips + concomitant CO2 fractional ablative laser resurfacing
99
Q

How can PRP/PRF and other aesthetic techniques be combined?

A

PRP is an autologous serum containing high concentrations of platelets and GF. Alpha granules within the platelets are responsible for promoting stem cell regeneration and soft tissue remodelling.

  • angiogenesis
  • neocollagenesis
  • adipogenesis

PRF - second generation of PRP, autologous platelets, leukocytes are present in a complex fibrin matrix

  • Fibrin clot traps circulating stem cells and bring to injured site
  • Stem cells converge on secretory phenotype
  • Vascular and tissue restoration
  • PRF - physiological fibrin support matriz
  • Act as net to stem cells
  • Helps with stem cell migration and proliferation

Have been combined with laser therapies, micro needling, dermal fillers, autologous fat grafting leading to improved aesthetic results