Module 7 Flashcards
(99 cards)
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
2
Q
What is molluscum contagiosum?
A
- Multiple, grouped, opaque plaques with a depressed centre
- Usually occur in children
3
Q
What is milia?
A
- 1mm spherical papules
- Very small, superficial infundibular cysts
- Occur on cheek and eyelids
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
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
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
7
Q
What is trichofolliculoma?
A
- Benign papule or nodule
- Face or scalp
- May be a central punctum with hair protruding from the surface
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
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
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
11
Q
What is xanthelasmata?
A
- Yellow, flat plaques usually found medial to eyelids
- Associated with hyperlipidaemia
- Tx with trichloroacetic acid
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
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
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
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
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)
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
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)
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
20
Q
What is a trichilemmal (pilar) cyst?
A
- Firm, spherical skin-coloured nodules
- Occur on scalp
- Tx: removal bu enucleation
21
Q
What is a infundibular (epidermoid) cyst?
A
- Found on face, neck and chest
- Small punctum
- Often rupture leading to chronic inflammation
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)
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
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
25
What is a mole?
- 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
26
How does location dictate type of mole?
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
27
What is congenital hairy naevus?
- 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
28
What is atypical melanocytes (dysplastic) naevus?
- 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
29
What is a spitz?
- 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
30
What is a halo?
- 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
31
What is Becker's naevus?
- much larger than most melanocytes naevi
- prescent in adolescent males
- flat, unilateral hyperpigmented area of skin
- upper back, chest or shoulder
- later becomes hairy
32
What is blue naevus?
- 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)
33
What is malignant melanoma?
- 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
34
What are the risk factors for malignant melanoma?
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
35
What are the clinicopathological variants of melanoma?
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
36
How to identify melanomas?
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
37
What is the most significant and consistent prognostic factor?
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
38
Survival rates of melanoma.
```
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
```
39
What is the recommended treatment for melanoma?
```
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
40
How does melanoma spread?
Lymphatic drainage system
41
How do you stage patients with intermediate thickness melanoma (1-4mm)?
Sentinel lymph node biopsy
42
What are the pre-cancerous lesions that can evolve into a SCC?
Actinic keratosis
| SCC in-situ (Bowen's disease, Erythroplasia of Queryat)
43
What is the median age of onset of SCC and BCC?
SCC - mid 70s
| BCC - late 60s
44
What are the risk factors for NMSC?
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
What is actinic keratosis?
- 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
What is SCC in situ?
- 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
What are the different types of BCC?
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
How do you diagnose BCC?
Punch biopsy
Incision
Excision
49
How are BCCs managed?
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
What factors affect prognosis of BCC?
High risk sites - nose, nasolabial folds, lips, ears, arounds eyes
Large tumours >2cm diameter
Recurrent tumours
Histologically, micro nodular or infiltrative tumours
51
What are the clinical features of SCC?
- 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
How is an SCC diagnosed?
Incisional or punch biopsy
53
What factors affect the metastatic potential of SCC?
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
How are SCCs managed?
- Excision with 4mm margin
- High risk require Mohs' micrographic surgery
- Radiotherapy - non-resectable tumours
- Regular follow up for 5 years
55
What is sclerotherapy?
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
What are the indications for sclerotherapy Tx:
- Varicose veins
- Low-flow vascular malformations
- Symptomatic hemangiomas
- Benign vascular tumours
- Telangiectasia or spider veins
- Reticular veins
57
Describe LL venous anatomy.
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
What is the pathophysiology of lower limb venous insufficiency?
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
What are varicose veins?
Ectatic, tortuous, dilated veins that are often associated with incompetent valves
At least 3mm in size
Increased risk of superficial vein thrombosis
60
What are telangiectasia?
Flat, red vessels smaller than 1mm in diameter
61
What are venules?
Blue, between 1-2mm
62
What are reticular veins?
2-4mm in diameter
63
How do you classify chronic venous disorders?
C - clinical manifestations
E - etiological factors
A - anatomic distribution
P - underlying pathophysiology
64
What are the different sclerosing agents?
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
How do you manage chronic venous in sufficiency?
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
What aspects of history should you ascertain before deciding on microsclerotherapy/sclerotherapy?
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
What are the symptoms of varicose veins?
```
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
What are symptoms of telangiectasia?
```
Burning
Cramping
Swelling
Throbbing
Leg fatigue
```
69
What should you look for on clinical examination of LL?
- 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
What investigations would you request for patients with chronic venous insufficiency?
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
What is the procedure for microsclerotherapy?
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
What are the advantages of foam sclerotherapy?
Minimally invasive and therefore fewer side effects
Easily repeatable
Low cost
73
What is post-procedure care for sclerotherapy?
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
What is dermabrasion?
The removal of a proportion of the dermis by abrasion
75
What are the different types of dermabrasion?
- Mechanical
- Manual
- Microdermabrasion
- Crystal
- Crystal free
76
What are the approaches to scar revision?
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
Describe mechanical dermabrasion.
- 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
Describe manual dermabrasion.
- Sterilised sandpaper
| - Simpler and cheaper
79
Describe microdermabrasion.
- 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
Define microneedling.
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
Describe collagen induction therapy.
- 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
What is cicatrisation?
Contraction of fibrous tissue at wound site by fibroblasts, leading to smaller scar but distorted tissue
83
Describe normal stimulation of collagen production.
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
What is a skin needling rolling device?
```
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
What are the indications for micro-needling?
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
What are the contraindications for micro-needling?
- 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
What is the method for micro-needling?
- 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
What is after care for micro-needling?
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
What are the disadvantages of micro-needling?
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
What are the effects of using Vitamin A and C during micro-needling?
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
How can radio-frequency be combined with other aesthetic methods?
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
How can botulinum toxin and fillers be combined?
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
How can acetyl-hexapeptide-3 and botox be combined?
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
How can micro needling and cosmeceuticals be combined?
Microneedling creates micro holes through SC, epidermis and dermis (depending on length) allowing penetration of cosmeceuticals into the skin
95
How can microdermabrasion and cosmeceuticals be combined?
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
How can US and cosmeceuticals be combined?
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
How can lasers and cosmeceuticals be combined?
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
How can surgery, lasers and filler be combined?
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
How can PRP/PRF and other aesthetic techniques be combined?
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
