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chapter 10 skin and subcutaneous tissue (chapter 40 bailey ) (1).pptx
- 1. Skin and subcutaneoustissues DR VIJAY JAGANATHAN MS MRCS DNB surgery MCh DNB plastic surgery fellow in hand and reconstructive microsurgery PROFESSOR ,Dept of Plastic surgery
- 2. Epidermis: • -5% ofthe skin • five layers - strata:basalis (deep), spinosum, granulosum, lucidum & corneum (superficial). • keratinised, stratified squamous epithelium; • -Keratinocytes grow and are replaced by mitoses in stratum granulosum • -strata lucidum; granulosum and spinosum: :Thick in glabrous skin and absent in eyelid skin.
- 3. Melanocytes : • dendriticcells / neural crest origin, • located in basal epidermis. • Melanin - transferred via membrane processes • transferred to keratinocytes in the strata granulosum and spinosum. • Ethnic diff in skin colour --By distribution of melanin in keratinocytes, not by number of it
- 4. Sweat glands Eccrine glands •distributed throughout the entire body surface • except in lips. • secrete sweat in response to emotion or during thermoregulation.
- 5. Apocrine glands • secretion.in response to emotion and hormone/ become active at puberty. • found in the axillae and groins • secretion,- malodourous after bacterial degradation, Sweat glands
- 7. angiosomes • 3d segmentsof tissue -with arterial & venous supply • Blood flows b/w neighbouring angiosomes by choke vessel • ‘choke’ vessels, - situated within muscles Blood supply to the skin anastomoses in subfascial, fascial, subdermal, dermal and subepidermal plexi.
- 8. • Epidermis hasno blood vessels/ cells nourish by diffusion. • venous drainage is via both valved and unvalved veins. • Unvalved veins allow oscillating flow in the subdermal plexus angiosomes
- 9. • Neurofibromatosis • Schwanncells form tumours • 70% -autosomal dominant /30% sporadic mutations. • Chromosomes 17 gene mutation Gardner’s syndrome • autosomal dominant disease • variant of familial adenomatous polyposis (FAP) • abnormal gene on Ch. 5. • multiple epidermoid cysts and lipomata.
- 10. Naevoid basal cellcarcinoma (Gorlin’s) syndrome • autosomal dominant • abnormal tumour suppressor gene on Ch. 9q 22-31 coding - ‘patched’ protein. • c/f multiple basal cell carcinomas (BCCs). • Head - over-developed supraorbital ridges; broad nasal roots; hyperteliorism; molar odontogeniccysts. • Trunk - bifid ribs; scoliosis; • Hand - brachymetacarpalism; palmar pits
- 11. Hyperhydrosis • excessive eccrinesweating • palms, soles of the feet, axillae and groins, treated • -antiperspirants • -local injections with botulinum toxin A. • - laparoscopic cervical sympathectomy.
- 12. Lipodystrophy • a localisedor generalised loss of fatty tissue, • complication of long-term administration of insulin, • treatment with protease inhibitors in hiv • transplant recipients. treated by • by autologous fat grafting, • injections of poly-L-lactic acid • free tissue transfer.
- 13. HIDRADENITIS SUPPURATIVA (HS •four women for every man • apocrine glands, • MC IN axillae and groins; • but also the scalp, breast, chest and perineum • genetic predisposition with variable penetrance, • associated with obesity and smoking.
- 14. Treatment • stop smoking •lose excess weight • antiseptic soaps • tea tree oil • non-compressive and aerated underwear. • antibiotics • antiandrogen drug • require radical excision & Reconstruction HIDRADENITIS SUPPURATIVA (HS
- 15. PYODERMA GANGRENOSUM (PG) •cutaneous ulceration with purple undermined edges, • secondary to IBD , RA, non-Hodgkin’s lymphoma or Wegener’s granulomatosis • respond to steroids • surgery may exacerbate the condition.
- 16. Necrotising fasciitis • Meleney’ssynergistic gangrene and Fournier’s gangrene are variants • synergistic, polymicrobial infection • MC streptococcal species (Group A β-haemolytic) C/F : • oedema beyond skin erythema; • & woody-hard texture OF SC tissues; • cant distinguish fascial plane & muscle; • disproportionate pain N skin vesicles & soft tissue crepitus • Lymphangitis - absent.
- 17. Xray air insc tissues Mx : • surgical – excise till bleeding tissues • antibiotics • VAC dressings, • early skin grafting Mortality - 30% and 50% Necrotising fasciitis
- 18. Milia • hard, keratinretention cysts • mc babies and chronic sun exposure, in the elderly Epidermal cysts/sebaceous cysts • LINED stratified-squamous epithelium, from hair follicle infundibuli • fixed to the skin + central punctum • excision if uninfected Meibomian cysts - epidermal cysts on edge of the eyelid • Tricholemmal cysts- from epidermis external root sheath of hair follicle
- 20. SKIN TUMOURS -Benign lesions Basal cell papilloma (seborrhoeic keratosis, senile keratosis, verruca senilis) • warty lesions • pigmented and hyperkeratotic • from the basal layer of epidermal cells • contain melanocytes. Papillary wart (verruca vulgaris)- • infection with human papilloma virus (HPV),hpv • also cause- plantar warts and condylomata acuminata.
- 21. • Freckle (ephelis)-containsa normal number of melanocytes,/large number of melanin granules • Nevus (mole )- non specific medical term for visible circumscribed lesion of skin or mucosa(cluster of melanocytes ) • Intradermal naevus- faintly pigmented papules /mc in adults / cluster of dermal melanocytes • compound nevus -dermoepidermal junctional proliferation of naevus cells, with dermis projection / mc in adolescent
- 22. naevus of Ota •MC Oriental and African races • four times MC in women • dermal, melanocytic hamartoma • blue or grey macule • mc site face trigeminal V1 and V2 dermatomes. naevus of Ito • dermal melanocytosis • MC shoulder • occur simultaneously with naevus of Ota
- 23. Tricholemmoma (naevus sebaceousof Jadassohn) • congenital hamartoma • appearance of a linear verrucous naevus. • 10% form a BCC Adenoma sebaceum (tuberous sclerosis, Bourneville disease) • facial papules (angiofibromas • in children before 10 years of age • MX ;argon or pulse dye lasers or scalpel Rhinophyma • end-stage sequela of nasal acne rosacea • C/F nasal sebaceous gland hypertrophy and hyperplasia • MC affect elderly men (M:F12:1). • Occult BCCs exist in 3%. • Treatment = dermabrasion or laser resurfacing
- 24. Extramammary Paget’s disease(intraepidermal adenoca) • Mc site axillae, genital and perianal • 25% there is in situ or invasive adenocarcinoma. Giant congenital pigmented naevus or giant hairy naevus • naevus cells -from epidermis to subdermal muscle. • precursors of melanoma, 3–5% • 1 in 3 childhood melanoma arise in GCPN, • Melanoma presentation in GCPN 15% at birth; 62% at puberty 99% by 45 yrs
- 25. Atypical (dysplastic) naevus •irregular proliferations of melanocytes at the basal layer of epidermis • Diagnostic c/f- 3 of below • variegated pigmentation • ill-defined borders; • undulating irregular surfaces • measure >5 mm. • types : sporadic or familial (familial atypical multiple mole- melanoma (FAMMM) syndrome). • Melanoma risk in dysplastic naevus • Sporadic : 6 times greater • fammm syndrome: 10% risk
- 26. Basal cell carcinoma •Malignant tumour of epithelial cells of basal epidermis and hair follicles; • MC men than women. • 95% cases - 40 and 80 yrs • 33% arise in parts of body not sunexposed • .Nodular and nodulocystic - 90% of BCC
- 27. Localized variety 1. nodular; 2.nodulocystic; 3. cystic; 4. pigmented and 5. naevoid generalised • superficial: 1.multifocal & 2.superficialspreading • infiltrative: 1.morphoeic,2. ice pick and 3. cicatrizing collagenase Basal cell carcinoma
- 28. high-risk’ • large (>2cm); • near the eye, nose and ear • Recurrent tumours • presence of immunosuppression • micronodular or infiltrating subtypes Basal cell carcinoma
- 29. two-stage surgical approachOR Mohs’ micrographic surgery IF • margins are ill-defined, or • tissue at a premium (nose, eyes) • excision margin between 2 and15 mm, depending on the macroscopic variant.
- 30. radiotherapy • elderly orinfirm patients, • similar recurrence rates to surgery • risk of generating further malignancy after 1–2 decades. 5-fluorouracil, imquimod • Biopsy-proven, • superficial tumours
- 31. SCC associated with •chronic inflammation (SCC IN scar -Marjolin’s ulcer.) • immunosuppression. • IR • chemical carcinogens (arsenicals, tar) • HPV 5 and 16 • current and previous tobacco use
- 32. SCC is acontinuum of lesion of • actinic (solar) Keratosis (AK), i.e. cutaneous horns • keratoacanthomas,
- 33. AKs • permananent sundamage • MICRO :dyskeratosis / partial-thickness, cellular atypia, / subepidermal inflammation / intact basement membrane • c/f : ‘wax and wane’ AS macular and papular lesion • • Can improve after moisturisation • upto 20% form SCC. • keratin horn: AK with a height greater than base diameter- / 10% has underlying SCC
- 34. Keratoacanthomas • self-healing SCCs •twice as common in men 50–70 • MC face or limbs • Othe factors : HPV in a hair follicle /smoking /chemical carcinogen. • Treatment :Excision not observation
- 35. Bowen’s disease • SCCin situ or dysplasia in hypertrophic AKs • MC -mucocutaneous surface of the body. • erythroplasia of Queyrat- glans penis bowens disease • treatment : • Topical therapy with 5-fluorouracil or imiquimod • surgical excision with a 4 mm margin, • Mohs’ micrographic surgery for larger or recurrent lesions
- 36. Better Prognosis : •Depth <2 mm, no metastasis worse prognosis • >6 mm, 15% -have metastasised. • Surface size: lesions >2 cm • higher the Broder’s grade • Microscopic invasion of lympho-vascular spaces or nerve • Scc on lips and ears have higher local recurrence • Extremities tumors fare worse than those on the trunk.
- 37. Treatment : • Surgicalexcision • margins for primary excision • 4 mm clearance for tumor <2 cm across, • 1-cm clearance margin if >2 cm. • 95% of local recurrence and regional metastases occur within 5 years
- 38. Cutaneous malignant melanoma •75% - skin malignancy-related deaths. • MC cancer in young adults (20–39 years) • 5% of MM second primary melanoma. Develops • 7% of MM presents as occult metastasis from an unknown primary
- 39. People at mostrisk of developing MM • genetic syndromes • past history of MM • first-degree relatives who have MM; • more than 30 sun-acquired naevi • history of five significant sun-burns before the age of 16 • fair-skinned/ red-haired people living close to the equator • excessive UVR exposure • anyone with immunosuppression
- 40. Transformation of nevito melanoma • 10–20% of MM form in pre-existing naevi, • MC naevi to form MM are atypical naevi, atypical junctional lenitiginous naevi (usually facial) giant pigmented congenital naevi.
- 41. Superficial spreading melanoma(SSM) • MC (70%) • usually arising in a pre-existent naevus • Nodularity within SSM MEANS onset of the vertical growth phase.
- 42. Nodular melanoma (NM) •15% of all MM • 5% amelanotic. • more aggressive than SSM, • MC arise de novo • MC men • MC trunk, head or neck • MC blue/black papules, 1–2 cm in diameter, sharply demarcated.{lack horizontal growth phase},
- 43. Lentigo maligna melanomaLMM • 5% and 10% of MM • slow-growing, • MC variegated brown macule • MC face, neck or hands of the elderly • MCwomen . • have less metastatic potential ( long time for verticalgrowth )
- 44. Acral lentigious melanoma •(2–8% of MM) • MC soles of feet and palms of hands. • rare in white-skinned individuals • MC Afro-Caribbean, Hispanic and Asian population (35–60%). • MC flat, irregular macule • 25% are amelanotic
- 45. Amelanotic melanoma • Flesh-coloured, • C/F : mets from unknown skin primary; or gastrointestinal tract, with obstruction or intussusception. Desmoplastic melanoma • MC head and neck region. • propensity for perineural infiltration • amelanotic clinically
- 46. Management : excision biopsy with2–3 mm margin of skin& a cuff of subdermal fat Sugical Margins for melanoma wide local excision • in situ melanoma- 5 mm margin • melanoma <1 mm deep- 1 cm margin • deeper lesions- 2 cm only margin Incision biopsy large lesions on the face where an excision biopsy of the whole lesion would be disfiguring
- 47. ADJUVANT THERAPY FOR UNRESECTABLEAND METASTATIC MM. dabrafenib or vemurafenib, block B-RAF action Trametinib different action on the MAPK ( mitogen activated protein kinase ) ipilimumab or nivolimumab immune checkpoint inhibitors
- 48. q True about epidermisis • 85% of the skin • keratinised,non stratified squamous epithelium; • Keratinocytes grow and are replaced by mitoses in stratum granulosum • granulosum and spinosum are Thin in glabrous skin
- 49. A • True aboutepidermis is • 85% of the skin • keratinised,non stratified squamous epithelium; • Keratinocytes grow and are replaced by mitoses in stratum granulosum • granulosum and spinosum are Thin in glabrous skin
- 50. Q • True aboutMelanocytes are • dendritic cells / neural crest origin, • located in spinosum epidermis. • Melanin - transferred by diapedisis • melanin, is transferred to keratinocytes in the strata granulosum and spinosum.
- 51. A • True aboutMelanocytes are • dendritic cells / neural crest origin, • located in spinosum epidermis. • Melanin - transferred by diapedisis • melanin, is transferred to keratinocytes in the strata granulosum and spinosum.
- 52. Q • ECCRINE GLANDSARE • SEBACEOUS GLANDS • distributed throughout the entire body surface, • Maximum glands are in lips. • secrete sweat in response to puberty hormones
- 53. a • ECCRINE GLANDSARE • SEBACEOUS GLANDS • distributed throughout the entire body surface • Maximum glands are in lips. • secrete sweat in response to puberty hormones
- 54. Q FALSE STATEMENT IS •Angiosomes are connected by choke vessels • Choke vessels are mainly in subdermal plexus • Oscillating veins are unvalved • Epidermis nourishes by simple diffusion
- 55. FALSE STATEMENT IS •Angiosomes are connected by choke vessels • Choke vessels are mainly in subdermal plexus • Oscillating veins are unvalved • Epidermis nourishes by simple diffusion
- 56. q Following are dueto abnormality in chromosome 9 except • Gardeners syndrome • Ferguson-Smith syndrome • Xeroderma pigmentosum • Gorlin’s syndrome
- 57. a Following are dueto abnormality in chromosome 9 except • Gardeners syndrome • Ferguson-Smith syndrome • Xeroderma pigmentosum • Gorlin’s syndrome
- 58. q • Treatment ofhyperhydrosis are all except • -antiperspirants • -local injections with botulinum toxin A. • - laparoscopic cervical sympathectomy. • Anticholinergic drugs
- 59. A • Treatment ofhyperhydrosis are all except • -antiperspirants • -local injections with botulinum toxin A. • - laparoscopic cervical sympathectomy. • Anticholinergic drugs
- 60. q All are trueabout lipodystrophy except • It’s a complication administration of insulin, • It’s a complication of hiv • Seen in transplant recipients. • treated by by autologous fat grafting, • treated by injections of poly-L-lactic acid • treated by free tissue transfer.
- 61. A All are trueabout lipodystrophy except • It’s a complication administration of insulin, • It’s a complication of hiv • Seen in transplant recipients. • treated by by autologous fat grafting, • treated by injections of poly-L-lactic acid • treated by free tissue transfer.
- 62. Q IN HIDRADENITIS SUPPURATIVA(HS) true is • four women for every man affected • Eccrine glandsaffected • Never happens in scalp, breast, chest and perineum • No genetic predisposition with variable penetrance, • Not associated with obesity and smoking. • Treatment with non-compressive and aerated underwear. • require radical excision & Reconstruction
- 63. A IN HIDRADENITIS SUPPURATIVA(HS) true is • four women for every man affected • Eccrine glands affected • Never happens in scalp, breast, chest and perineum • No genetic predisposition with variable penetrance • Not associated with obesity and smoking. • Treatment with non-compressive and aerated underwear. • require radical excision & Reconstruction
- 64. Q ALL EXCEPT ONEHIGHLY ASSOCIATED TO CAUSE PYODERMA GANGRENOSUM (PG) • IBD • RA • non-Hodgkin’s lymphoma • Wegener’s granulomatosis • SLE
- 65. A ALL EXCEPT ONEHIGHLY ASSOCIATED TO CAUSE PYODERMA GANGRENOSUM (PG) • IBD • RA • non-Hodgkin’s lymphoma • Wegener’s granulomatosis • SLE
- 66. q FALSE ABOUT Necrotisingfasciitis IS • It’s a polymicrobial infection • MC streptococcal species (Group A β-haemolytic) • Lymphangitis present • Xray air in sc tissues • early skin grafting treatment of choice
- 67. a FALSE ABOUT Necrotisingfasciitis IS • It’s a polymicrobial infection • MC streptococcal species (Group A β-haemolytic) • Lymphangitis present • Xray air in sc tissues • early skin grafting treatment of choice
- 68. Q False statement are •Milia are hard, keratin retention cysts &mc babies • sebaceous cysts lined with true, stratified-squamous epithelium, from external root sheath of hair follicle • Meibomian cysts - epidermal cysts on edge of the eyelid • Tricholemmal cysts- from epidermis of hair follicle infundibuli
- 69. A False statement are •Milia are hard, keratin retention cysts &mc babies • sebaceous cysts lined with true, stratified-squamous epithelium, from external root sheath of hair follicle • Meibomian cysts - epidermal cysts on edge of the eyelid • Tricholemmal cysts- from epidermis of hair follicle infundibuli
- 70. Q False statement inthis is • Papillary wart (verruca vulgaris)- HPV associated • Basal cell papilloma (seborrhoeic keratosis)- contain melanocytes • Freckle (ephelis)- normal number of melanocytes,/large number of melanin granules • Intradermal naevus -cluster of dermal melanocytes • compound nevus -Subcutaneous proliferation of naevus cells, with dermis projection
- 71. A False statement inthis is • Papillary wart (verruca vulgaris)- HPV associated • Basal cell papilloma (seborrhoeic keratosis)- contain melanocytes • Freckle (ephelis)- normal number of melanocytes,/large number of melanin granules • Intradermal naevus -cluster of dermal melanocytes • compound nevus -Subcutaneous proliferation of naevus cells, with dermis projection
- 72. q • True statementare • naevus of Ota MC shoulder • naevus of Ito is hamartoma • Naevus of ito cant occur simultaneously with naevus of Ota • naevus of Ota mc site face trigeminal V1 and V2 dermatomes.
- 73. a • True statementare • naevus of Ota MC shoulder • naevus of Ito is hamartoma • Naevus of ito cant occur simultaneously with naevus of Ota • naevus of Ota mc site face trigeminal V1 and V2 dermatomes.
- 74. Q • False statementamong premalignant conditions • Adenoca exists insitu in exramammary pagets disease • Dysplastic nevi is only sporadic • Giant hairy navi 99 % after 45 years have melanoma • Famm is associated with dysplastic nevi
- 75. A • False statementamong premalignant conditions • Adenoca exists insitu in exramammary pagets disease • Dysplastic nevi is only sporadic • Giant hairy navi 99 % after 45 years have melanoma • Famm is associated with dysplastic nevi
- 76. q • Treatment ofbcc are all except • 5-fluorouracil, • imquimod • radiotherapy • Mohs’ micrographic surgery • Surgery with margin b/w 10 and15 mm always
- 77. A • Treatment ofbcc are all except • 5-fluorouracil, • imquimod • radiotherapy • Mohs’ micrographic surgery • Surgery with margin b/w 10 and15 mm always
- 78. Q • FOLLOWING STATEMENTSARE WRONG ABOUT SCC • expresses cytokeratins 1 and 10. • HPV 5 and 16 can cause them • Keratoacanthomas is a self healing scc • In keratin horn 10% has underlying SCC • Bowen’s disease treated with 4 mm marginexcision • >6 mm depth invasion -50 % -have metastasised.
- 79. a • FOLLOWING STATEMENTSARE WRONG ABOUT SCC • expresses cytokeratins 1 and 10. • HPV 5 and 16 can cause them • Keratoacanthomas is a self healing scc • In keratin horn 10% has underlying SCC • Bowen’s disease treated with 4 mm marginexcision • >6 mm depth invasion -50 % -have metastasised.
- 80. q • True statementsabout cutaneous malignant melanoma are • 10%- skin malignancy-related deaths. • MC cancer in young adults (20–39 years) • 50%of MM second primary melanoma • 70% of MM presents as occult metastasis from an unknown primary
- 81. a • True statementsabout cutaneous malignant melanoma are • 10%- skin malignancy-related deaths. • MC cancer in young adults (20–39 years) • 50%of MM second primary melanoma • 70% of MM presents as occult metastasis from an unknown primary
- 82. q • Propensity forperineural infiltration is for • Desmoplastic melanoma • Amelanotic melanoma • Nodular melanoma (NM) • Acral lentigious melanoma
- 83. a • Propensity forperineural infiltration is for • Desmoplastic melanoma • Amelanotic melanoma • Nodular melanoma (NM) • Acral lentigious melanoma
Editor's Notes
- #3 Epidermis: -5% of the skin -five layers - strata:basalis (deep), spinosum, granulosum, lucidum & corneum (superficial). -keratinised, stratified squamous epithelium; -Keratinocytes grow and are replaced by mitoses in stratum granulosum -strata lucidum; granulosum and spinosum: :Thick in glabrous skin and absent in eyelid skin.
- #5 Eccrine glands distributed throughout the entire body surface,except in lips. secrete sweat in response to emotion or during thermoregulation. Apocrine glands secretion. in response to emotion and hormone/ become active at puberty. found in the axillae and groins secretion,- malodourous after bacterial degradation,
- #10 Neurofibromatosis Schwann cells form tumours 70% -autosomal dominant /30% sporadic mutations. Chromosomes 17 gene mutation Naevoid basal cell carcinoma (Gorlin’s) syndrome autosomal dominant abnormal tumour suppressor gene on Ch. 9q 22-31 coding - ‘patched’ protein. c/f multiple basal cell carcinomas (BCCs). Head - over-developed supraorbital ridges; broad nasal roots; hyperteliorism; molar odontogeniccysts. Trunk - bifid ribs; scoliosis; Hand - brachymetacarpalism; palmar pits Xeroderma pigmentosum abnormality on the ‘patched’ gene of Ch. 9q aberrant nucleotide repair during cellular DNA maintenance .>2000-fold increase in skin cancer risk autosomal recessive (60% mortality by 20 years of age). Gardner’s syndrome autosomal dominant disease variant of familial adenomatous polyposis (FAP) abnormal gene on Ch. 5. multiple epidermoid cysts and lipomata. Ferguson-Smith syndrome autosomal-dominantly / Ch. 9q abnormality develop multiple self-healing squamous cell carcinomas (SCC).
- #14 Lipodystrophy a localised or generalised loss of fatty tissue, complication of long-term administration of insulin, treatmen with protease inhibitors in hiv transplant recipients. treated by by autologous fat grafting, injections of poly-L-lactic acid free tissue transfer.
- #15 HIDRADENITIS SUPPURATIVA (HS)
- #18 Necrotising fasciitis Meleney’s synergistic gangrene and Fournier’s gangrene are variants synergistic, polymicrobial infection;MC streptococcal species (Group A β-haemolytic) C/F : oedema beyond skin erythema; & woody-hard texture OF SC tissues; cant distinguish fascial plane & muscle; disproportionate pain N skin vesicles & softtissue crepitus Lymphangitis - absent. Xray air in sc tissues Mx : surgical – excise till bleeding tissues , antibiotics ,VAC dressings, early skin grafting Mortality - 30% and 50%
- #28 Basal cell carcinoma Malignant tumour of epithelial cells of basal epidermis and hair follicles; MC men than women. 95% cases - 40 and 80 yrs 33% arise in parts of body not sunexposed .Nodular and nodulocystic - 90% of BCC Main Predisposing factor – UVR / sun exposure, Other predisposing factors arsenic,coal tar, aromatic hydrocarbons, ionising radiation and genetic skin cancer syndromes. BCC is divided into Localized variety :1. nodular;2. nodulocystic;3. cystic;4. pigmented and 5. naevoid generalised -superficial: 1.multifocal & 2.superficial spreading; infiltrative: 1.morphoeic,2. ice pick and 3. cicatrizing microscopic 26 subtypes Diagnostic : ovoid cells in nests with a single ‘palisading’ layer. only the outer layer divide, Morphoeic BCCs synthe size type 4 collagenase and so spread rapidly Prognosis ; 1.‘low-risk’ 2,high-risk’ large (>2 cm); (near the eye, nose and ear); Recurrent tumours; presence of immunosuppression; micronodular or infiltrating subtypes. MANAGEMENT two-stage surgical approach OR Mohs’ micrographic surgery IF margins are ill-defined, or tissue at a premium (nose, eyes) excision margin between 2 and15 mm, depending on the macroscopic variant. recurrence rate –67% if margins grossly + / 33% microscopic + or reported ‘close’ radiotherapy elderly or infirm patients, similar recurrence rates to surgery risk of generating further malignancy after 1–2 decades. 5-fluorouracil, imquimod Biopsy-proven, superficial tumours Follow-up is reserved for Lesion In high-risk areas; in sun-damaged skin; with syndromes; in who decline further surgery after incomplete excisions.
- #31 recurrence rate –67% if margins grossly + / 33% microscopic + or reported ‘close’
- #47 horizontal growth phase, cells spread along the dermo-epidermal junction /migration is radial. vertical growth phase: dermis maybe invaded.
- #49 ADJUVANT THERAPY FOR UNRESECTABLE AND METASTATIC MM. 50% of MM has B-RAF V600 mutations. dabrafenib or vemurafenib, Targeted therapy in stage IV melanoma promising results block B-RAF action Trametinib different action on the MAPK ( mitogen activated protein kinase )- stops cell growth & promotes apoptosis. Combined use with dabrafenib counter acquired tumour resistance via MAPK pathway reactivation, good results in stage 4 disease. ipilimumab or nivolimumab immune checkpoint inhibitors good result in metastatic or unresectable melanoma.
- #56 angiosomes 3d segments of tissue -with an arterial supply and a venous drainage. Blood flows between neighbouring angiosomes by choke vessels ‘choke’ vessels, - situated within muscles. Blood supply to the skin anastomoses in subfascial, fascial, subdermal, dermal and subepidermal plexi. Epidermis has no blood vessels/ cells nourish by diffusion. venous drainage is via both valved and unvalved veins. Unvalved veins allow oscillating flow in the subdermal plexus