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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5192_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Dedications
- •Contributors
- •Acknowledgments
- •Preface
- •1 Basic science
- •1.1 Structure and function of the skin
- •Epidermis
- •Cellular biology of the epidermis
- •Dermal cells of importance
- •Structural components and cell biology of the dermis
- •1.2 Embryology
- •1.3 Wound healing
- •Dermis
- •1.4 Genetics
- •Basic cell biology of genome
- •Inheritance patterns
- •1.5 Ultraviolet light
- •Ultraviolet light (Fig. 1.8)
- •Minimal erythema dose
- •1.6 Immunology
- •Innate immunity
- •Adaptive immunity
- •1.6.2 Immunologic mediators
- •Cytokines
- •Pattern recognition receptors
- •Antimicrobial proteins (AMPs)
- •The complement system
- •B cells
- •T cells (majority of lymphocytes)
- •Innate lymphoid cells
- •NK cells
- •Mononuclear phagocytes
- •Langerhans cells
- •Dendritic cells
- •Mast cells
- •Eosinophils
- •Neutrophils
- •1.6.4 Major histocompatibility complex
- •1.7 Laboratory techniques
- •1.7.1 Tissue acquisition and processing
- •Polymerase chain reaction (PCR)
- •Quantitative reverse transcriptase PCR (qRT-PCR)
- •16S ribosomal RNA (rRNA) sequencing
- •DNA sequencing
- •RNA sequencing
- •Fluorescence in situ hybridization (FISH)
- •Immunohistochemistry (IHC)
- •Enzyme-linked immunosorbent assay (ELISA)
- •1.7.3 Cellular engineering and gene therapy
- •2 Dermatopharmacology
- •2.1 ANTIHISTAMINES
- •Mechanism
- •Other antihistamines
- •Introduction
- •Mucocutaneous
- •Systemic
- •Teratogenicity
- •Contraindications
- •Interactions
- •2.3 CORTICOSTEROIDS
- •Hypothalamic-pituitary-adrenal (HPA) axis suppression (Box 2.1)
- •Psychiatric changes
- •Contraindications
- •Pregnancy
- •Clinical use
- •Intramuscular CS
- •Pulse IV CS
- •Adalimumab
- •Certolizumab pegol
- •Golimumab
- •Indications
- •Ustekinumab
- •IL-17 inhibitors
- •IL-23 inhibitors
- •Spesolimab
- •Rituximab
- •IL-1 inhibitors
- •Omalizumab
- •Dupilumab
- •Lebrikizumab and tralokinumab
- •Nemolizumab
- •Vismodegib and sonidegib
- •Intralesional CS
- •Monitoring
- •2.4 IMMUNOMODULATORY AGENTS
- •Apremilast and other PDE-4 inhibitors
- •Janus Kinase (JAK) and Tyro inhibitors
- •Agents used in dermatology
- •Laboratory monitoring
- •Azathioprine
- •Important monitoring points
- •Cyclosporine
- •Important pharmacology points
- •Indications
- •Important monitoring points
- •Methotrexate
- •Important pharmacology points
- •Indications and contraindications
- •Important monitoring points
- •Important pharmacology points
- •Indications
- •Monitoring guidelines
- •Cytotoxic agents
- •Hydroxyurea
- •Cyclophosphamide
- •Chlorambucil
- •Antimalarial agents
- •Important pharmacology points
- •Indications
- •Dapsone
- •Important pharmacology points
- •Indications
- •Important monitoring points
- •Etanercept
- •MEK inhibitors (trametinib, cobimetinib, binimetinib)
- •Ipilimumab
- •PD-1 inhibitors (pembrolizumab, nivolumab, cemiplimab) and PD-L1 inhibitors (avelumab, atezolizumab)
- •Imatinib mesylate
- •Ibrutinib
- •Talimogene
- •Mechlorethamine hydrochloride
- •Brentuximab vedotin
- •Mogamulizumab
- •Romidepsin and vorinostat
- •2.6 ANTIMICROBIAL AGENTS
- •Topical antibacterial agents
- •Bacitracin
- •Benzoyl peroxide
- •Metronidazole
- •Azelaic acid
- •Systemic antibacterial agents
- •Penicillins
- •Polymyxin B
- •Neomycin
- •Mupirocin
- •Retapamulin
- •Gentamicin
- •Iodoquinol
- •Cephalosporins
- •Vancomycin
- •Macrolides
- •Fluoroquinolones
- •Tetracyclines
- •Clindamycin
- •Carbapenems
- •Linezolid
- •Daptomycin
- •Others
- •Antiviral agents
- •Acyclovir
- •Valacyclovir
- •Famciclovir and penciclovir
- •Foscarnet
- •Bleomycin
- •Podophyllin resin and podophyllotoxin
- •Cantharidin
- •Sinecatechins
- •5-Fluorouracil and imiquimod (discussed in section 2.5)
- •I. Azoles
- •Itraconazole
- •Fluconazole
- •Ketoconazole
- •Voriconazole
- •Posaconazole
- •Miconazole, clotrimazole, and econazole
- •Efnaconazole
- •Luliconazole
- •II. Allylamines/benzylamines
- •Terbinafne
- •Butenafne
- •IV. Ciclopirox olamine
- •VI. Nystatin
- •VIII. Tavaborole
- •Antiparasitic agents (Tables 2.7 and 2.8)
- •2.7 PHOTOTHERAPY
- •UVA modalities
- •Psoralen plus UVA (PUVA)
- •UVA-1 (340–400 nm)
- •UVB modalities
- •Extracorporeal photochemotherapy
- •Photodynamic therapy (PDT)
- •2.8 MISCELLANEOUS AGENTS
- •Sunscreens
- •Topical cosmetic agents
- •Bimatoprost
- •Brimonidine and oxymetazoline
- •Hydroquinone
- •Psychiatric agents
- •Antiandrogens and androgen inhibitors
- •Spironolactone
- •Finasteride and dutasteride
- •Combination oral contraceptive pills
- •Clascoterone
- •Calcipotriene and calcitriol
- •Attenuated androgens
- •Danazol and stanozolol
- •Colchicine
- •Potassium iodide
- •Thalidomide
- •Topical calcineurin inhibitors
- •Pimecrolimus and tacrolimus
- •Intravenous immunoglobulin (IVIG)
- •Glycopyrrolate
- •Oxybutynin
- •Botulinum toxin
- •Aluminum chloride
- •2.9 DRUG INTERACTIONS AND THE CYTOCHROME P-450 SYSTEM
- •Key points
- •CYP1A2
- •CYP2C9
- •CYP2D6
- •CYP3A4 (most relevant to dermatologists)
- •Classic CYP mnemonics
- •2.10 DRUG REACTIONS
- •Urticaria, angioedema, and anaphylaxis
- •Fixed drug eruption/Stevens-Johnson syndrome/toxic epidermal necrolysis
- •Drug-induced hypersensitivity syndrome/drug reaction with eosinophilia and systemic symptoms (DIHS/DRESS)
- •Acute generalized exanthematous pustulosis (AGEP)
- •Photosensitive drug reactions
- •Drug-induced pigmentary changes
- •Bullous drug reactions, lichenoid drug eruptions, drug-induced connective tissue disease
- •Other drug eruptions
- •3 General dermatology
- •3.1 Papulosquamous dermatoses
- •3.2 Eczematous dermatoses
- •3.3 Interface dermatitis
- •Vacuolar interface dermatitis
- •Autoimmune connective tissue disease (AICTD)
- •Erythema multiforme (EM)
- •Stevens-johnson syndrome (SJS), and toxic epidermal necrolysis (TEN, lyell’s syndrome)
- •Pityriasis lichenoides
- •Fixed drug eruption (FDE)
- •Graft- versus- host disease (GVHD)
- •Lichenoid interface dermatitis
- •Lichen planus (LP)
- •Keratosis lichenoides chronica (KLC)
- •Erythema dyschromicum perstans (ashy dermatosis)
- •Lichenoid keratosis (benign lichenoid keratosis [BLK], LP-like keratosis)
- •Lichen nitidus
- •3.4 Blistering diseases
- •Pemphigus disease family
- •Pemphigus vulgaris (PV)
- •Pemphigus foliaceus (PF)
- •Paraneoplastic pemphigus (PNP)/paraneoplastic autoimmune multiorgan syndrome (PAMS)
- •Autoimmune subepidermal blistering diseases
- •Bullous pemphigoid (BP; pemphigoid)
- •Mucous membrane pemphigoid (MMP; cicatricial pemphigoid)
- •Linear IgA bullous dermatosis/chronic bullous disease of childhood (LABD/CBDC)
- •Epidermolysis bullosa acquisita
- •Bullous systemic lupus erythematosus
- •Dermatitis herpetiformis (duhring disease)
- •Inherited blistering diseases
- •Epidermolysis bullosa (see chapter 4)
- •Darier disease (keratosis follicularis)
- •Other blistering diseases
- •Lupus band test (LBT)
- •Lupus erythematosus
- •Chronic cutaneous lupus erythematosus (CCLE)
- •Subacute cutaneous lupus erythematosus
- •Acute cutaneous lupus erythematosus (ACLE)
- •Other rare cutaneous lupus variants
- •Systemic lupus erythematosus (SLE)
- •Drug-induced SLE (DI-SLE)
- •Lupus-related diseases
- •Other autoimmune connective tissue diseases and sclerosing dermopathies
- •Dermatomyositis (DM)
- •Sjögren’s syndrome
- •Relapsing polychondritis
- •Mixed connective tissue disease (MCTD)
- •Rheumatoid arthritis
- •Systemic-onset juvenile idiopathic arthritis (still’s disease)
- •Morphea (localized scleroderma)
- •Eosinophilic fasciitis (shulman syndrome)
- •Abnormalities of connective tissue
- •3.6 Granulomatous/histiocytic disorders
- •Non-infectious granulomas
- •Granuloma annulare (GA)
- •Annular elastolytic giant cell granuloma (actinic granuloma of O’Brien
- •Interstitial granulomatous dermatitis and arthritis (IGDA) and palisaded neutrophilic granulomatous dermatitis (PNGD)
- •Interstitial granulomatous drug eruption
- •Necrobiosis lipoidica (necrobiosis lipoidica diabeticorum, NLD)
- •Necrobiotic xanthogranuloma (NXG)
- •Cutaneous crohn’s disease
- •Sarcoidosis
- •Histiocytoses
- •Langerhans cell histiocytosis (LCH)
- •Non-langerhans cell histiocytoses (discussed in Table 3.23)
- •Malignant histiocytic disorders
- •3.7 Monoclonal gammopathies of dermatologic interest
- •3.8 Xanthomas
- •3.9 Urticaria and angioedema
- •3.10 Neutrophilic dermatoses
- •Amicrobial pustulosis of the folds
- •3.11 Eosinophilic disorders
- •Granuloma faciale
- •Eosinophilic folliculitis
- •Papuloerythroderma of ofuji
- •Wells’ syndrome (eosinophilic cellulitis)
- •Hypereosinophilic syndrome (HES)
- •3.12 Figurate erythemas
- •3.13 Follicular and eccrine/apocrine disorders
- •Acne variants
- •Acne fulminans
- •Acne conglobata
- •Solid facial edema in acne
- •Acne mechanica
- •Neonatal acne (neonatal cephalic pustulosis)
- •Infantile acne
- •Transverse nasal crease
- •Acne in setting of endocrinologic abnormality
- •Acne cosmetica
- •Pomade acne
- •Chloracne
- •Radiation acne
- •Acneiform eruptions
- •Drug-induced acne
- •Acne-associated syndromes
- •SAPHO (chronic recurrent multifocal osteomyelitis)
- •PAPA
- •HAIR-AN
- •Apert syndrome (acrocephalosyndactyly)
- •Rosacea
- •Epidemiology
- •Rosacea subtypes
- •Erythematotelangiectatic (vascular)
- •Phymatous
- •Ocular
- •Rosacea variants
- •Solid facial edema in rosacea (morbihan disease and rosacea lymphedema)
- •Pyoderma faciale (rosacea fulminans)
- •Granulomatous rosacea
- •Lupus miliaris disseminatus faciei
- •Folliculitis
- •Gram-negative folliculitis
- •Hot tub folliculitis
- •Eosinophilic folliculitis
- •Disseminate and recurrent infundibulofolliculitis
- •Viral-associated trichodysplasia
- •Pseudofolliculitis barbae
- •Acne keloidalis nuchae
- •Follicular occlusion tetrad (acne conglobata, hidradenitis suppurativa, dissecting cellulitis of the scalp, and pilonidal cyst)
- •Hidradenitis suppurativa (acne inversa)
- •Pilonidal cyst
- •Dissecting cellulitis of the scalp and acne conglobata (discussed in alopecia and acne sections)
- •Other diseases of eccrine and apocrine sweat glands
- •Hyperhidrosis
- •Hypohidrosis and anhidrosis
- •Miliaria
- •Bromhidrosis
- •Chromhidrosis
- •Fox-fordyce disease (apocrine miliaria)
- •3.14 Drug reactions
- •3.15 Photodermatoses and other physical dermatoses
- •Temperature-related dermatoses
- •Thermal burns
- •Erythema ab igne
- •Cold injuries
- •Photoaging
- •Polymorphous light eruption
- •Hydroa vacciniforme (see Chapter 4)
- •Actinic folliculitis
- •Chronic actinic dermatitis
- •Actinic prurigo (see chapter 4)
- •Solar urticaria
- •Mechanical injuries
- •3.17 Neurodermatology and psychodermatology
- •Cutaneous manifestations of psychiatric illness or self-induction
- •Delusions of parasitosis
- •Excoriation disorder (neurotic excoriations)
- •Factitial dermatitis/dermatitis artefacta
- •Gardner-diamond syndrome
- •Body dysmorphic disorder
- •Cupping/coining
- •Other neurocutaneous dermatoses
- •Scalp dysesthesia/burning scalp syndrome
- •Burning mouth syndrome
- •Brachioradial pruritus
- •Notalgia paresthetica
- •Meralgia paresthetica
- •Trigeminal trophic syndrome
- •Familial dysautonomia/riley-day syndrome
- •Auriculotemporal nerve syndrome (frey syndrome)
- •3.18 Palmoplantar keratodermas
- •3.19 Nutritional disorders in dermatology
- •3.21 Ulcers (Table 3.33)
- •3.22 Vasculitides, vasculopathies, and other vascular disorders
- •Subtypes of cutaneous small vessel vasculitis
- •Henoch-schonlein purpura (HSP)
- •Epidemiology
- •Pathophysiology
- •Clinical presentation
- •Key features of adult HSP
- •Key features of childhood HSP
- •Treatment
- •Laboratory testing: See CSVV section
- •Pathology
- •Acute hemorrhagic edema of infancy (Fig 3.86)
- •Epidemiology
- •Pathophysiology
- •Clinical presentation
- •Treatment
- •Urticarial vasculitis
- •Epidemiology
- •Pathophysiology
- •Clinical presentation
- •Pathology
- •Laboratory testing
- •Treatment (Table 3.41)
- •Erythema elevatum diutinum
- •Epidemiology
- •Pathophysiology
- •Clinical presentation
- •Pathology
- •Treatment
- •Mixed cryoglobulinemia (see cryoglobulinemia section)
- •Small to medium vessel vasculitis
- •Granulomatosis with polyangiitis (wegener)
- •Epidemiology
- •Pathophysiology
- •Clinical presentation
- •Pathology
- •Treatment
- •Microscopic polyangiitis (MPA)
- •Epidemiology
- •Pathophysiology
- •Clinical presentation
- •Pathology
- •Laboratory testing: See CSVV, especially:
- •Treatment
- •Eosinophilic granulomatosis with polyangiitis (churg-strauss syndrome)
- •Epidemiology
- •Pathophysiology
- •Clinical presentation: Three classic stages (Table 3.47)
- •Pathology
- •Laboratory testing
- •Treatment
- •Medium vessel vasculitis
- •Subtypes: PAN and kawasaki’s disease
- •Polyarteritis nodosa
- •Epidemiology
- •Pathophysiology
- •Clinical presentation
- •Pathology
- •Laboratory testing: See CSVV
- •Treatment
- •Kawasaki disease (acute febrile mucocutaneous lymph node syndrome)
- •Epidemiology
- •Pathophysiology
- •Clinical presentation (Fig. 3.90)
- •Laboratory testing
- •Treatment
- •Key testing facts
- •Large vessel vasculitis
- •Subtypes: Temporal arteritis and Takayasu’s arteritis
- •Temporal arteritis (giant cell arteritis)
- •Epidemiology
- •Pathophysiology
- •Clinical presentation
- •Pathology
- •Laboratory workup
- •Treatment
- •Takayasu’s arteritis
- •Epidemiology
- •Pathophysiology
- •Clinical presentation
- •Pathology
- •Laboratory workup
- •Treatment
- •Summary of organ system involvement in various vasculitides (Table 3.49)
- •Cryoglobulinemias
- •Epidemiology
- •Thrombosis and thrombotic syndromes
- •Important subtypes
- •Calciphylaxis
- •Antiphospholipid syndrome
- •Epidemiology
- •Pathophysiology
- •Clinical presentation
- •Pathology
- •Treatment
- •Pathogenesis
- •Clinical presentation
- •Pathology
- •Treatment
- •Other vasculopathies (Table 3.51)
- •Other vascular disorders
- •Venous lake
- •Telangiectasia
- •Erythromelalgia
- •Livedo reticularis (LR)
- •Angiospastic macules (bier spots)
- •3.23 Panniculitides and lipodystrophies
- •3.24 Dermatoses of pregnancy
- •3.25 Hair, nail, and mucosal disorders
- •Non-scarring alopecia
- •Androgenetic alopecia
- •Trichotillomania
- •Alopecia areata
- •Temporal triangular alopecia
- •Congenital atrichia with papules
- •Cicatricial (scarring) alopecia
- •Central centrifugal cicatricial alopecia
- •Lichen planopilaris
- •Acne keloidalis nuchae
- •Dissecting cellulitis of the scalp (perifolliculitis capitis abscedens et suffodiens)
- •Folliculitis decalvans
- •Traction alopecia
- •Hair shaft abnormalities
- •Hypertrichosis and hirsutism
- •Hypertrichosis
- •Nail disorders
- •Mucosal disorders
- •3.26 Pigmentary disorders
- •Disorders of hypopigmentation and depigmentation
- •Vitiligo
- •Halo nevus
- •Chemical and physical agent-induced hypopigmentation
- •Idiopathic guttate hypomelanosis
- •Progressive macular hypomelanosis
- •Nevus anemicus
- •Pigmentary mosaicism
- •Hypomelanosis of ito
- •Nevus depigmentosus
- •Disorders of hyperpigmentation
- •Melasma
- •Erythema dyschromicum perstans (ashy dermatosis) discussed in Section 3.3
- •Lichen planus pigmentosus
- •Linear and whorled nevoid hypermelanosis
- •Prurigo pigmentosa
- •Familial progressive hyperpigmentation
- •Endocrinopathies
- •Pigmentary demarcation lines (aka futcher’s lines, voight lines, ito’s lines)
- •4 Pediatric dermatology
- •4.1 Neonatal dermatology
- •4.2 Viral exanthems and select infectious disorders of childhood
- •4.3 Inherited pigmentary disorders
- •Hypo-/depigmentation
- •Pigmentary mosaicism
- •Oculocutaneous albinism (OCA)
- •Silvery hair syndromes
- •Griscelli syndrome
- •Hermansky-Pudlak syndrome
- •Piebaldism
- •Waardenburg syndrome
- •Hyperpigmentation
- •McCune-Albright syndrome
- •Lentiginoses syndromes
- •Hereditary dyschromatoses
- •Dyschromatosis symmetrica hereditaria (acropigmentation of Dohi)
- •Dyschromatosis universalis hereditaria
- •Naegeli-Franceschetti-Jadassohn syndrome (NFJS)/dermatopathia pigmentosa reticularis (DPR)
- •4.4 Epidermolysis bullosa
- •4.5 Tumor syndromes
- •4.6 Vascular tumors, malformations, and related vascular disorders
- •Vascular tumors
- •Phace syndrome
- •LUMBAR/SACRAL syndrome
- •Multiple hemangiomas
- •Kasabach-Merritt phenomenon
- •Vascular malformations
- •Capillary malformations (CM)
- •Sturge-Weber syndrome (encephalotrigeminal angiomatosis)
- •Phakomatosis pigmentovascularis
- •Phakomatosis pigmentokeratotica
- •PIK3CA-related overgrowth spectrum (PROS)
- •Klippel-trenaunay syndrome
- •Macrocephaly capillary malformation syndrome
- •Cloves syndrome
- •Proteus syndrome
- •Beckwith-wiedemann syndrome
- •Diffuse capillary malformation with overgrowth (DCMO)
- •Venous malformations
- •Maffucci syndrome (enchondromas with multiple angiomas)
- •Blue rubber bleb nevus syndrome
- •Glomulovenous malformations (GVMs; previously termed “glomangiomas”)
- •Lymphatic malformations
- •Macrocystic lymphatic malformations (cystic hygroma)
- •Gorham-stout (disappearing bone) disease
- •Congenital lymphedema (hereditary congenital lymphedema, Nonne-Milroy syndrome)
- •Arteriovenous malformations
- •AVMs
- •Parkes-weber syndrome
- •Cobb syndrome (cutaneomeningospinal angiomatosis)
- •Other vascular disorders
- •4.7 Disorders of hair and nails
- •Pachyonychia congenita
- •Ectodermal dysplasias
- •Hypohidrotic ectodermal dysplasia (Christ-Siemens-Touraine syndrome)
- •Hidrotic ectodermal dysplasia (Clouston syndrome)
- •Ectodermal dysplasias due to p63 mutation
- •Schöpf-Schulz-Passarge syndrome
- •Other disorders
- •Rubinstein-Taybi syndrome
- •Parakeratosis pustulosa
- •Congenital malalignment of the great toenails
- •4.8 Inherited metabolic and nutritional disorders
- •4.9 Inherited connective tissue disorders
- •4.10 Autoinflammatory disorders (periodic fever syndromes)
- •4.12 Premature aging syndromes and DNA repair disorders
- •4.13 Primary immunodeficiency disorders with cutaneous manifestations
- •4.14 Disorders of cornification
- •Actinic prurigo
- •Diaper dermatitis
- •Juvenile plantar dermatosis
- •Acropustulosis of infancy
- •Trichorhinophalangeal syndrome
- •Midas syndrome (also MLS or microphthalmia with linear skin defects)
- •H syndrome
- •Cutaneous mastocytosis
- •Neutrophilic eccrine hidradenitis of childhood
- •5 Infectious diseases
- •5.1 Viral diseases
- •Herpes simplex virus (HHV-1/HSV-1 and HHV-2/HSV-2)
- •Varicella zoster virus (VZV; HHV-3)
- •Epstein-Barr virus (HHV-4)
- •Cytomegalovirus (HHV-5)
- •HHV-6 (Roseola infantum, exanthem subitum, sixth disease)
- •HHV-7
- •HHV-8
- •Poxviruses
- •Zika virus
- •Dengue virus
- •Viral hepatitides (Table 5.2)
- •Viral-associated trichodysplasia of immunosuppression
- •COVID-19
- •5.2 HIV/AIDS dermatology
- •5.3 Bacterial infections
- •Staphylococcal skin infections
- •Corynebacterial skin infections
- •Clostridium skin infections
- •Filamentous bacteria
- •Other gram-positive infections
- •Pseudomonas
- •Bartonella
- •Rickettsia
- •Other gram-negative skin infections
- •Borrelia
- •Nonvenereal (endemic) treponematoses
- •Syphilis
- •Cutaneous tuberculosis
- •Leprosy (hansen’s disease)
- •Atypical mycobacteria
- •Tinea versicolor (pityriasis versicolor)
- •Piedra
- •Tinea nigra
- •Sporotrichosis
- •Lobomycosis
- •Mycetoma (madura foot)
- •Chromoblastomycosis
- •Histoplasmosis
- •Blastomycosis (“north American blastomycosis”)
- •Coccidioidomycosis
- •Paracoccidioidomycosis (“South American blastomycosis”)
- •Candidiasis
- •Cryptococcosis
- •Aspergillosis
- •Fusarium
- •Penicilliosis
- •Zygomycosis (mucormycosis)
- •Phaeohyphomycosis
- •Protothecosis
- •Rhinosporidiosis
- •5.5 Parasites and other creatures
- •Parasitic infestations
- •Scabies
- •Lice
- •Tungiasis
- •Myiasis
- •Protozoa
- •Leishmaniasis
- •Toxoplasmosis
- •Helminths
- •Cutaneous larva migrans
- •Larva currens
- •Onchocerciasis (“river blindness”)
- •Loiasis
- •Filariasis
- •Swimmer’s itch and seabather’s eruption
- •Trichinosis
- •Dracunculiasis (guinea worm)
- •Gnathosomiasis
- •Cysticercosis
- •Cutaneous amebiasis
- •Free-living amoeba
- •Gi-associated amoeba
- •Bites and stings
- •Biting and stinging insects
- •Arachnids (ticks, mites, spiders, and scorpions)
- •Millipedes and centipedes
- •Snake bites
- •6 Neoplastic dermatology
- •Neoplastic dermatology
- •6.1 Keratinocytic neoplasms
- •Premalignant/malignant
- •Actinic keratosis (AK)
- •Bowen’s disease (squamous cell carcinoma in situ)
- •Invasive cutaneous squamous cell carcinoma (cSCC, “SCC”)
- •Verrucous carcinoma
- •Keratoacanthoma
- •Basal cell carcinoma
- •6.2 Cysts
- •6.3 Melanocytic neoplasms
- •6.4 Adnexal neoplasms and hamartomas
- •Comparative dermatopathologic features of sweat gland neoplasms for board exam purposes
- •Poroma (classic juxtaepidermal type)
- •Hidroacanthoma simplex
- •Dermal duct tumor
- •Hidradenoma
- •Spiradenoma
- •Cylindroma
- •Syringoma
- •Mixed tumor (MT; “chondroid syringoma”)
- •Hidradenoma papilliferum (HPAP)
- •Syringocystadenoma papilliferum (SPAP, SCAP)
- •Papillary eccrine adenoma (PEA)
- •Tubular apocrine adenoma (TAA)
- •Porokeratotic eccrine ostial and dermal duct nevus
- •Microcystic adnexal carcinoma (MAC)
- •Aggressive digital papillary adenocarcinoma (ADPA)
- •Adenoid cystic carcinoma (ACC)
- •6.5 Hair follicle neoplasms/hamartomas
- •Folliculo-sebaceous-apocrine hamartomas
- •Trichofolliculoma
- •Fibrofolliculoma
- •Nevus sebaceus
- •Neoplasms with follicular germinative differentiation
- •Trichoepithelioma
- •Neoplasms with follicular matrix differentiation
- •Pilomatricoma (calcifying epithelioma of malherbe)
- •Neoplasms with follicular sheath (trichilemmal) differentiation
- •Trichilemmoma
- •Desmoplastic trichilemmoma (DTL)
- •Tumor of the follicular infundibulum (TFI)
- •Trichoadenoma (TA; of Nikolowski)
- •Proliferating pilar (trichilemmal) tumor
- •6.6 Sebaceous proliferations
- •6.7 Neural neoplasms
- •6.8 Smooth muscle neoplasms
- •6.9 Hematolymphoid neoplasms
- •6.10 Fibrohistiocytic neoplasms
- •Multinucleate cell angiohistiocytoma
- •Nodular fasciitis
- •Fibrous hamartoma of infancy
- •Giant cell tumor of tendon sheath (tenosynovial giant cell tumor)
- •Connective tissue nevus (collagenoma and elastoma)
- •6.11 Vascular proliferations
- •Benign vascular lesions
- •Vascular malformation (includes “port wine stain,” “cavernous hemangioma” old terminology)
- •Intravascular papillary endothelial hyperplasia (masson tumor, pseudoangiosarcoma)
- •Angiokeratoma
- •Infantile hemangioma
- •Pyogenic granuloma (lobular capillary hemangioma)
- •Epithelioid hemangioma (angiolymphoid hyperplasia with eosinophils, ALHE)
- •Targetoid hemosiderotic lymphatic malformation (hobnail hemangioma, targetoid hemosiderotic hemangioma)
- •Tufted angioma
- •Glomeruloid hemangioma
- •Glomus tumor/glomangioma
- •Borderline vascular neoplasms
- •Kaposiform hemangioendothelioma
- •Kaposi sarcoma (KS)
- •Other borderline vascular neoplasms (rare; not commonly tested)
- •High-grade malignant vascular neoplasms
- •Angiosarcoma
- •Vascular neoplasm associations
- •6.12 Neoplasms of adipocytic lineage
- •6.13 Dermoscopy
- •Seborrheic keratosis
- •Actinic keratosis
- •Basal cell carcinoma
- •Squamous cell carcinoma in situ
- •Squamous cell carcinoma
- •Ink spot lentigo
- •Vascular lesions (e.g., cherry angiomas)
- •Hemorrhage
- •Porokeratosis
- •Sebaceous hyperplasia
- •Dermoscopic patterns of melanocytic lesions
- •7 Dermatopathology
- •7.1 Essential concepts in dermatopathology
- •7.2 High-yield dermatopathology diagnoses at a glance
- •7.3 High-yield dermatopathology differential diagnoses
- •8 Dermatologic surgery
- •8.1 Surgical anatomy
- •8.2 Local anesthetics and perioperative pain control
- •8.3 Surgical instruments and needles
- •8.4 Suture techniques
- •8.5 Wound closure materials
- •8.7 Electrosurgery
- •8.8 Cryosurgery
- •8.9 Excisions
- •8.10 Mohs surgery
- •8.11 Flaps
- •8.12 Grafts
- •8.13 Surgical complications and measures to avoid them
- •8.14 Scar improvement
- •8.15 Nail surgery
- •8.16 Wound dressings
- •9 Cosmetic dermatology
- •9.1 Lasers

7.3 High-Yield Dermatopathology Differential Diagnoses
Fig. 7.67 Cutaneous polyarteritis nodosa. The affected small arteries in the upper subcutis show marked brin extravasation into their walls. Only a tiny amount
of inammation tends to spill into fat lobules that are in immediate proximity to
the affected vessels n
vasculopathic reaction pattern. In: Weedon’s Skin Pathology. 5th ed. Elsevier.
2021:241–304.)
very mild lobular panniculitis. (From Patterson JW. The
Table 7.32 High-Yield Vascular Tumors
Masson’s/IPEH Papillary projections of bland
Angiosarcoma Poorly-formed vessels filled with RBCs
Glomeruloid hemangioma Round nodules comprised of capillaries
Angiolymphoid hyperplasia
with eosinophilia/epithelioid
hemangioma
Kaposi sarcoma Bloody “busy dermis ” spindled
IPEH, intravascular papillary endothelial hyperplasia
endothelial cells around hyaline
cores; well-circumscribed (not a
feature seen in malignant vascular
neoplasms); arises within large
thrombosed vessel (weird
papillary-like appearance is due
to re-canalizing of vessel)
(Fig. 7.69)
and lined by large, dark, atypical
endothelial cells that protrude into
the lumen in a “piled-on” fashion;
NOT well-circumscribed
(Fig. 7.70)
contained within a large dilated
vascular space in the dermis →
resembles renal glomerulus; part of
POEMS syndrome
Lymphoid nodules 1 TONS of
eosinophils around thick-walled
vessels with large “epithelioid”
endothelial cells often w/
intracytoplasmic vacuoles
(Fig. 7.71)
cells with adjacent slit-like vessels,
“promontory sign” (vessels forming
around vessels), ↑ plasma cells,
↑ hemosiderin and siderophages (See
Fig. 7.22)
Fig. 7.68 Pancreatic panniculitis. Characteristic “ghost” cells, neutrophils, and
basophilic calcication are seen.
Table 7.31 High-Yield Neural Tumors
Neurofibroma (NF) “Seagull”-shaped wavy nuclei in bubble
Plexiform neurofibroma Wavy fascicles of NF embedded in myxoid
Schwannoma Encapsulated SQ nodule, Antoni A/B areas,
Palisaded encapsulated
neuroma (solitary
circumscribed neuroma)
Traumatic neuroma Small nerve fascicles surrounded by scar
Nerve sheath myxoma
(“Neurothekeoma”)
gum pink stroma; scattered mast cells
background of diffuse NF
hyalinized ectatic vessels within tumor
Well-circumscribed, pesudoencapsulated
superficial dermal nodule comprised of
nerve fascicles separated by clefts
tissue
Myxoid lobules of spindled cells in dermis
surrounded by fibrous septa
Fig. 7.69 Intravascular papillary endothelial hyperplasia. “Pseudoangiosarcoma”
appearance is due to re-canalization of a thrombus within a large vessel (helpful
clue = look for the old vessel wall surrounding the well-circumscribed lesion).
435

CHAPTER 7 • Dermatopathology
Fig. 7.70 Angiosarcoma. Observe the “dissecting vascular spaces” that appear
to be cutting the dermis into multiple pieces. Vascular spaces are poorly-formed
and leaky (results in hemorrhagic/bruise-like clinical appearance), and lined by
atypical, hyperchromatic endothelial cells with a “piled-on” appearance. Some of
the tumor cells appear to be free-oating in the vascular spaces.
Fig. 7.71 Angiolymphoid hyperplasia with eosinophilia (epithelioid hemangioma).
Nodular proliferation of vessels lined by plump epithelioid endothelial cells. A
orid inammatory inltrate of lymphocytes and eosinophils is present. (From
Buehler D, Billings SD. Soft tissue tumors and tumor-like reactions. In: Busam
KJ, ed. Dermatopathology: A Volume in the Series: Foundations in Diagnostic
Pathology, 2nd ed. Philadelphia: Elsevier; 2016, pp 513-594.)
Table 7.33 High-Yield Adipocytic Tumors
Disease Key Features
Lipoma Solely mature lipocytes with small eccentric nuclei
Mobile encapsulated lipoma Lobules of necrotic fat enclosed within fibrous capsule
Angiolipoma Lipoma with capillary proliferation; capillaries filled w/ fibrin thrombi
Pleomorphic lipoma Mature lipocytes among myxoid matrix with interspersed ropey collagen, bland spindle cells, and floret giant cells
Spindle cell lipoma
Hibernoma Multivacuolated tumor cells, not as pink or grainy-appearing as granular cell tumor. Lipocytes look like small berries
Nevus lipomatosus superficialis Mature lipocytes infiltrating the superficial dermis; similar, but more extreme features seen in Goltz syndrome
Table 7.34 High-Yield Smooth Muscle DDx
Accessory nipple Central pore-like structure, deep mammary (modified apocrine) glands and scattered smooth muscle bundles
Becker’s nevus
Piloleiomyoma Haphazardly arrayed smooth muscle fascicles in superficial-mid dermis
Angioleiomyoma Round, well-circumscribed pink nodule with compressed vascular lumen in deep dermis/subcutis
Leiomyosarcoma Hypercellular proliferation of spindled smooth muscle cells w/ atypical, hyperchromatic nuclei and mitoses. Deep tumors are more
Table 7.35 DF Versus DFSP Versus Fibromatosis
DF Dermal-based spindle cell neoplasm with “ curlicue” pattern, collagen trapping (most obvious at periphery), overlying epidermal/
DFSP Densely cellular dermal and SQ tumor w/ storiform pattern, infiltrates deep into SQ fat enveloping lipocytes in a “honeycomb”
Fibromatosis Long “sweeping” fascicles of myobroblasts with wavy corkscrew nuclei and wavy collagen
Looks like epidermal nevus 1 smooth muscle hamartoma together with terminal hairs
aggressive than tumors located entirely within the dermis.
follicular induction, and hemosiderin-laden GCs and histiocytes ; 1/– significant hemorrhage (aneurysmal DF); Never infiltrates
deeply into fat!; factor XIIIa
pattern; CD341, factor XIIIa , stromelysin-3 , and t(17;22) translocation (detectable by FISH) (Fig. 7.72)
Inclusion body bromatosis (infantile digital broma) has characteristic perinuclear eosinophilic inclusions
(main distinguishing feature from spindle cell lipoma!); CD341, S100 negative, loss of RB1 in ~100% of cases ("RB1deleted soft tissue tumor family" = spindle cell lipoma/pleomorphic lipoma, pleomorphic fibroma, atypical spindle cell/
pleomorphic lipomatous tumor, and other less common entities; loss of RB1 distinguishes from liposarcoma )
Mature lipocytes among myxoid matrix containing spindle cells and interspersed ropey collagen, CD341 S100–,
loss of RB1 in ~100% of cases ("RB1-deleted soft tissue tumor family" = spindle cell lipoma/pleomorphic lipoma,
pleomorphic fibroma, atypical spindle cell/pleomorphic lipomatous tumor, and other less common entities; loss of RB1
distinguishes from liposarcoma)
1
, stromelysin-31, and CD34
436

7.3 High-Yield Dermatopathology Differential Diagnoses
A B
Fig. 7.72 Dermatobrosarcoma protuberans (DFSP). (A) Low power shows a spindle-cell neoplasm in the dermis. (B) High power shows so-called honeycombing in
the fat.
Table 7.36 Amorphous “Pink Stuff in Dermis” DDx
Amyloid (macular/lichen) Sparse pink deposits of amyloid ( AK type) in superficial dermis, melanophages, no inflammation (Fig. 7.73)
Amyloid (nodular) Fissured, pale pink amyloid (AL type) material in superficial to mid dermis, and abundant plasma cells (distinguishes
Colloid milium Fissured, pale pink deposits completely filling/expanding superficial-mid dermis (deeper than macular/lichen
Erythropoietic protoporphyria Dermal deposits of pink material; hyaline cuff around superficial vessels, no solar elastosis (because patients diligently
Lipoid proteinosis
AL, light chain-derived amyloid; BMZ, basement membrane zone; PAS-D, periodic acid-Schiff with diastase; EPP, erythropoietic protoporphyria
from colloid milium) (Fig. 7.74)
amyloid); extensive solar elastosis (adult form only); no inflammation (vs. nodular amyloid) (Fig. 7.75)
avoid sun) (Fig. 7.76)
Pink hyaline BMZ material (type IV collagen; PAS-D1) predominantly centered around superficial and deep (deeper than
EPP) vessels and adnexae, with “onion skin” pattern (Fig. 7.77)
Fig. 7.73 Macular amyloid. (From Brinster NK, Liu V, Diwan AH, McKee PH.
Cutaneous amyloidosis. In: Dermatopathology: A Volume in the High Yield Pa-
thology Series. Philadelphia: Elsevier, 2011, pp 278-280.)
Fig. 7.74 Nodular amyloid. (From Ferringer T. Metabolic disorders. In: Elston DM,
Ferringer T, eds. Dermatopathology, 3rd ed. Philadelphia: Elsevier, 2019; pp 251-263.)
437

CHAPTER 7 • Dermatopathology
Fig. 7.75 Colloid milium. Fissured pale-pink deposits ll and expand the supercial
and mid dermis. Lacks lymphoplasmacytic inammation (vs nodular amyloid).
Fig. 7.76 Erythropoietic protoporphyria. (From Ferringer T. Metabolic disorders.
In: Elston DM, Ferringer T, eds. Dermatopathology. 3rd ed. Philadelphia: Elsevier;
2019:251–263.)
Fig. 7.77 Lipoid proteinosis. Pink, hyaline BMZ material (Type IV collagen) forms
“onion skin” deposits around vessels in supercial and deep dermis (deeper than
EPP).
438

7.3 High-Yield Dermatopathology Differential Diagnoses
Table 7.37 Immediate Pattern Recognition Diagnoses
Chondrodermatitis
nodularis chronicus
helicis
Coma blister
Cutaneous endometriosis Well-formed glands of varying sizes, lined by pseudostratified columnar epithelium and surrounded by endometrial stroma
Elastosis perforans
serpiginosa
Giant cell tumor
of tendon sheath
Granular cell tumor
Myofibroma/
myopericytoma
Nevus sebaceus Papillomatosis overlying increased number of sebaceous glands directly opening onto epidermis; terminal hairs replaced
Nodular fasciitis Circumscribed nodule located in deep dermis/SQ; stellate myofibroblasts w/ “ tissue culture” appearance set in loose
Ochronosis Yellow-brown “bananas” in superficial dermis
Pseudoxanthoma elasticum
Sweet syndrome Dense neutrophilic infiltrate with karyorrhexis in dermis and marked papillary dermal edema; tissue cultures and bug stains
Verruciform xanthoma Verrucous hyperplasia with xanthoma cells stuffed in dermal papillae and superficial dermis ( Fig. 7.82)
PEH, pseudoendothelial hyperplasia; HPC, hemangiopericytoma
Ulcer w/ adjacent epidermal acanthosis, underlying reparative change, fibrin, vascular ectasia, and eosinophilic degenerated
cartilage
Paucicellular/noninflammatory subepidermal bulla, diffuse epidermal necrosis n subepidermal bulla, and sweat gland necrosis
(differentiates from SJS/TEN) (Fig. 7.78)
(basaloid cells in fibromyxoid background); RBCs and hemosiderin within and surrounding glands. No atypia (unlike cutaneous
mets of endometrial cancer) (Fig. 7.79)
Elastic fibers (stains black with VVG) spiraling through narrow serpiginous channel in epidermis
Deep tumor arising from tendon, containing innumerable multinucleate osteoclast-like giant cells, and fibrotic pink stroma
(Fig. 7.80)
PEH 1 pink cells in dermis w/ granular cytoplasm and round pustulo-ovoid bodies of Milian
Dermal-SQ tumor w/ multiple blue-gray (cartilage-colored) hypocellular nodules surrounded by hypercellular areas
containing “HPC-like” “staghorn” vessels (Fig. 7.81)
by apocrine glands
myxoid stroma with foci of hemorrhage and inflammation
Fragmented purple elastic fibers in dermis (VVG1 , von Kossa1)
MUST be negative!
A B
Fig. 7.78 Coma blister. (A) Pauci-inammatory subepidermal separation. (B) Basophilic necrosis of eccrine glands.
439

CHAPTER 7 • Dermatopathology
Fig. 7.79 Endometriosis of the umbilicus. Glands and stroma are set in brous
tissue. The glands are functional with some luminal hemorrhage.
Fig. 7.81 Myobroma. Biphasic tumor composed of hypocellular, blue-grey
myoid nodules surrounded by immature mesenchymal cells and hemangiopericytoma-like vascular spaces.
Fig. 7.80 Giant cell tumor of tendon sheath. (From Elston DM, Ko CJ, Ferringer
T. Fibrous tumors. In: Elston DM, Ferringer T, eds. Dermatopathology, 3rd ed.
Philadelphia: Elsevier, 2019; pp 350-392.)
440
A
B
Fig. 7.82 (A) and (B) Verruciform xanthoma. Mnemonic 5 “wart with foam cells
in dermal papillae.”

Table 7.38 High-Yield Infectious Diseases
HPV-induced lesions
Verruca Vulgaris
Myrmecia (Fig. 7.83)
Verruca plana (Fig. 7.84)
Verruca plana with EDV changes (Fig. 7.85)
Verrucous carcinoma (Fig. 7.86)
Histiocytic inclusions
“His GIRL Penelope”: Histoplasmosis, Granuloma Inguinale, Rhinoscleroma, Leishmaniasis/Leprosy, Penicillium
Infections with endospores
Rhinosporidiosis (“spores as big as a rhino!”) (Fig. 7.87)
Coccidioidomycosis (Fig. 7.88)
7.3 High-Yield Dermatopathology Differential Diagnoses
Fig. 7.83 Verruca with myrmecial changes (“myrmecial wart”). Compared with
verruca vulgaris, this entity has more extreme hyperkeratosis, epidermal
hyperplasia, and bright pink-purple inclusion bodies.
Fig. 7.84 Verruca plana. Minimal papillomatosis (vs VV), mild hypergranulosis,
supercial clear-colored koilocytes.
Fig. 7.85 Verruca plana with changes characteristic of epidermodysplasia verruciformis. Distinguished from normal verruca plana by presence of blue-gray
color of upper portion of epidermis.
Fig. 7.86 Verrucous carcinoma. (From Elston DM. Malignant tumors of the epidermis. In: Elston D, Ferringer T, eds. Dermatopathology. 3rd ed. Philadelphia:
Elsevier; 2019:54–67.)
441

CHAPTER 7 • Dermatopathology
Fig. 7.87 Rhinosporidiosis: individual spores mature to form small trophic cysts.
(From Grayson W, Calonje E. Infectious diseases of the skin. In: Calonje E, Brenn
T, Lazar AJ, Billings SD, eds. McKee’s Pathology of the Skin with Clinical Cor-
relations. 5th Ed. Philadelphia: Elsevier; 2020:826–975.)
Fig. 7.88 Coccidioidomycosis. Multiple spherules are present with surrounding
chronic inammation.
442

8
Dermatologic Surgery
Phillip C. Hochwalt and Thomas L.H. Hocker
CONTENTS LIST
8.1 SURGICAL ANATOMY
8.2 LOCAL ANESTHETICS AND PERIOPERATIVE PAIN CONTROL
8.3 SURGICAL INSTRUMENTS AND NEEDLES
8.4 SUTURE TECHNIQUES
8.5 WOUND CLOSURE MATERIALS
8.6 ANTISEPSIS AND STERILIZATION
8.7 ELECTROSURGERY
8.8 CRYOSURGERY
8.9 EXCISIONS
8.10 MOHS SURGERY
8.11 FLAPS
8.12 GRAFTS
8.13 SURGICAL COMPLICATIONS AND MEASURES TO AVOID THEM
8.14 SCAR IMPROVEMENT
8.15 NAIL SURGERY
8.16 WOUND DRESSINGS
8.1 SURGICAL ANATOMY
• Skin lines
■
Langer’s lines: skin lines that orient in the direction of
the natural gape of a wound after puncture with a
circular spike; lines run parallel to underlying muscles
Different than relaxed skin tension lines (RSTLs);
frequently perpendicular to them, in fact
■
RSTLs (Kraissl and Borges lines): lines that run
perpendicular to underlying muscles; most elective
incisions should be made parallel to these lines
• Head and neck anatomy
■
Arterial supply (Fig. 8.1)
Face supplied by external AND internal carotid:
♦ External carotid: supplies lateral, mid, and lower
face; most important branches include:
Supercial temporal artery: anterior and
parietal branches; supplies temple, scalp, and
lateral forehead
Maxillary artery: gives rise to:
Infraorbital artery: exits infraorbital
foramen; supplies mid face; anastomoses
with the internal carotid-derived arteries
(supratrochlear and supraorbital arteries)
Mental artery: exits mental foramen;
supplies chin and lower lip
Facial artery: gives rise to:
Labial arteries (inferior and superior):
supplies lips, columella, and ala
Angular artery: extension of facial artery
starting near base of ala (susceptible to
intraarterial ller injection); eventually
ends in anastomoses with branches of the
internal carotid (dorsal nasal artery
specically) near medial canthus
♦ Internal carotid: supplies mid forehead and
nasal root; anastomoses with branches of the
external carotid in the area of the medial canthus
and dorsal nose
Ophthalmic artery: responsible for most of
the facial arteries supplied by the internal
carotid. It travels through the optic canal into
the orbit where it supplies the retinal,
supraorbital and supratrochlear (axial artery
required for paramedian forehead ap),
infratrochlear, dorsal nasal (anastomoses with
angular artery), external nasal, anterior and
posterior ethmoidal, and lacrimal branches.
These branches supply the retina, forehead,
upper dorsal nose, and eyelids
Branches of the ophthalmic artery
anastomose heavily with those supplied by
the external carotid system
443

CHAPTER 8 • Dermatologic Surgery
Superficial temporal artery
Anterior branch
Parietal branch
Supratrochlear artery
Supraorbital artery
Zygomatico-orbital artery
Angular artery
Transverse facial artery
Superior labial artery
Facial artery
Inferior labial artery
Fig. 8.1 Arterial blood supply of the face. (From Salasche SJ. Anatomy. In: Rohrer TE, Cook JL, Nguyen TH, eds. Flaps and Grafts in Dermatologic Surgery. Philadel-
phia: Elsevier; 2007:1–14.)
These anastomoses are important when
inadvertent intraarterial injection of
steroids or llers occurs. Inadvertent
intraarterial injection of ller (glabellar
area most commonly) carries risk of
blindness due to retrograde movement of
ller to ophthalmic artery and
Sensory nerves are located supercial to SMAS
→ often transected during facial surgery →
numbness
■
Sensory nerves (Tables 8.1–8.2 and Figs. 8.2–8.4)
Cranial nerve (CN) V (trigeminal nerve): almost
wholly responsible for sensory innervation of face
♦ Boards factoids: Damage to CN V may result in
embolization into retinal artery
■
Venous system
Veins typically follow their associated arteries
Facial vein can communicate w/ cavernous sinus of
♦ Clinical pearl: injection of anesthetic into the
brain via pterygoid plexus or ophthalmic vein
♦ Danger triangle: area extending from corners of
the mouth to nasal root; infections in this area
can cause septic cavernous sinus thrombosis,
meningitis, and brain abscesses
■
Lymphatic system
Important for skin cancer mets; drainage can be
variable
♦ Upper and lateral face → parotid, preauricular,
and infraauricular nodes
♦ Lower and medial face → submandibular nodes
♦ Central lower lip and chin → submental nodes
♦ Lateral cervical nodes collect from the above areas
■
Supercial musculoaponeurotic system (SMAS)
Cervical plexus: supplies sensory innervation to
neck and occipital scalp
Sensory innervation of ear is complex
■
Motor innervation (Tables 8.3 and 8.4; Fig. 8.5)
Muscles of facial expression are innervated by
CN VII (facial nerve); facial muscles receive motor
innervation from their undersurface
♦ Boards factoid: as a minor function, CN VII
Composed of muscles and fascia of the face and neck;
allows for coordinated facial movement and helps
contain infection and cancer; contiguous w/ galea
Motor nerves all run deep to SMAS (penetrate
muscles from undersurface) → staying above SMAS
during facial surgery prevents motor nerve damage
Facial nerve emerges from stylomastoid foramen,
travels within the parotid gland and then splits into
ve branches: temporal, zygomatic, buccal,
mandibular, and cervical branches (“To Zanzibar By
Motor Car”)
Dorsal nasal artery
Anterior ethmoidal artery
Infraorbital artery
Buccal artery
Mental artery
trigeminal trophic syndrome and Frey’s
syndrome; CN V also supplies motor innervation
to muscles of mastication
supraorbital, supratrochlear, infraorbital, and
mental foramens will result in prolonged
anesthesia for vast majority of face (exceptions 5
parts of nose and angles of mouth)
also provides sensory input for anterior tongue
(via chorda tympani branch) and a small amount
of external auditory meatus
444
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