Tuesday, September 12 (ellen)

Dermatological Pathologies – Tuesday, September 12, 2006 Review of Normal Physiology Functions: physical barrier, absorption, thermoregulation, protection from UV (melanocytes), antibacterial activities (IgA), sensation Layers: ~ epidermis (basal cell layer with reproductive activity; at the bottom) ~ as they grow they accumulate keratin ~ dermis – has appendages (sweat glands, hair follicles, sebaceous glands, endocrine secretary glands) ~ has nerve endings ~ has collagen ~ adipose tissue Naturopathic Concepts of Dermatology Lesions on outside start often from manifestations inside ~ ex: psoriasis (if suppress the symptoms of this, you may never get to locate the root cause, which may actually be GI problem) ~ LI is paired with LU in TCM and LU manifests on skin Herring’s Law – disease moves from outward in but healing moves inward out ~ for NDs it’s a good sign if you are treating an organ that is deep down and then the px develops a skin lesion Look at entire body and the px’s environment Remember look at diet, start with elimination diet Terminology (not testable) Primary Lesions – appear first 1) Flat Lesion Macule – can determine from surrounding tissue by colour ~ ex: freckles 2) Elevated Solid Lesions Papule – can palpate, less than 5mm across, may or may not differ by colour Nodule – more than 5 mm, tend to be dome shaped Plaque – elevated with flat top, more than 5mm 3) Elevated Fluid-filled Lesions Vesicle – contains fluid, 5mm or less Bulla – contains fluid, larger than 5 mm Pustule – has pus Secondary Lesions – occur because original lesion was there 1) Scale – dry, horny, result of imperfect cornifications (production of keratin layer) 2) Lichenification – skin markings, eczema, usually due to chronic rubbing or scratching 3) Excoriation – breakage in epidermis, usually due to scratch 4) Hyperkeratosis/Acanthosis – hyperplasia (thickening) of epidermis, often a result of trauma 5) Spongiosis – intracellular edema of the epidermis (accumulation of fluid in epidermis)

Disorders of Hair Follicles Acne vulgaris Acne rosacea: damaged blood vessels b/c of constant dilation due to stimuli ~ vessels to dilate too easily and stay dilated for longer periods of time or remain permanently dilated  flushing and redness. ~ immune cells and inflammatory mediators causing papules ~ usually affects central face, eyes, and neck Folliculitis: inflammation of follicles ~ something gets into hair follicles and it gets inflamed ~ can evolve into boils, cysts, cellulites Usually Staph aureus is cause of inflammation Acne Vulgaris Open comedomes ~ non-inflmmatory ~ black heads ~ follicular papules with black keratin plug (due to sebum and keratin) ~ black because sebum is oxidized ~ generally not harmful, EXCEPT if it is in danger zone on face, and it drains into cavernous sinus which drains directly into CNS Closed comedomes ~ inflammatory (think pus) ~ bacteria Proprionibacterium acnes causes lipase degradation of sebaceous oils to form irritating fatty acids ~ trapped keratin plug  inflammation  erythema, papules, nodules, pustules ~ the more you squeeze, the more you damage the follicle, which means you create a bigger inflammatory response next time In relation to ND ~ skin health is more important than what you eat (ie: chocolate, fatty foods) ~ vitamin A is very important (might need to give toxic doses – so watch for pregnancy and liver damage) ~ can apply tea tree oil for topical antimicrobial, but more important to support immune and skin health ~ support anti-inflammatory fatty acids (fish oils) ~ vitamin C for skin healing ~ selenium for free radical scavenging ~ increase testosterone? Especially due to stress ~ too much simple sugar/refined CHO  insulin surge  eventually make you habituated to insulin Bollous Diseases ~ blisters! Pemphigus vulgaris Bullous pemphigoid Both are autoimmune

Pemphigus vulgaris IgG against own intercellular adhesion molecules Lysis of epithelial intercellular adhesions (desmosomes) Cause the two adjacent cells to “puff” up Get fragile suprabasal blister (above basal cell layer) and rupture easily which means increase risk of infection Bullous Pemphigoid Usually affects elderly Autoimmune ~ IgG to basement membrane Destruction of connection between dermis and epidermis (hemidesmosomes – attach basal cells to basal membrane) ~ basal cell lifted off dermis Tense subepidermal blister – not as fragile Urticaria (hives) Antigen sensitization (IgE) ~ maybe autoimmune, so then the IgE is formed against the mast cell and not necessarily antigen IgE causes mast cell degranulation – which releases histamine (which causes dermal vascular hyperpermeability) ~ mast cells tend to be higher concentration around small blood vessels Dermal edema and prurities Papules  plaques (Wheals – usually itchy) Keep in mind to look at food and gut health and stress related concerns (depresses immune function; changes peristalsis patterns, hormone cycles, bowel flows, etc) Can have delayed hives (takes time for leukocytes to get to the site of reaction) TCM  wind heat, wind damp ~ itchy is usually wind ~ heat because firing, irritated read Inflammatory Conditions Dermatitis (eczema) Psoriasis Pityriasis rosea Lichen Planus Eczematous Dermatitis Can be caused by: allergic contact, atopic, drug-related, Photoeczematous (UV light), and/or Primary irritant Starts with antigen stimulation Inflammatory infiltrate into dermis and epidermis Fluid separates keratinocytes Dermal edema and vesicle formation (very itchy) Body tries to heal by: Hyperkeratosis (thickening of epidermal layer) and acanthosis

Result of itching and scratching: Possible lichenification and excoriation Psoriasis Damage to stratum corneum leads to exposure to antigens, creates an antibody-mediated response Over time, these lesions contribute to abnormally reactive endothelium ~ lesions have typical silver-white loosely adherent scales Lymphocytes may induce angiogenesis in the dermis and keratinocyte growth Can be associated with: myopathies, enteropathies, AIDS, arthritis Lesions are well demaracated, pink, with signs of acanthosis Pityriasis rosea Pink flaky oval shaped rash Onset may be linked to viral infection Lichen Planus Self-limiting disease – leaves postinflammatory hyperpigmentation T-cells and Langerhans infiltrate the junction between dermis and epidermis Causes basal cell degeneration and necrosis See hyperplasia and immune injury to basal cells Pruritic, purple, polygonal papules  plaques  acanthosis, hyperkeratosis Lesions are symmetrical and have white dots (Wickham striae) Atopic Dermatitis Viewed as a hypersensitivity reaction Skin tends to be dry, hyperkeratotic, and easily lichenified  becomes chronic Risk factors: not breast fed, urban environment, hygiene, diet, poor digestive health, histamine release (are the mast cells stable or not? – function of diet ), “emotional tension”