Chronic And Infectious Dermatoses Flashcards
Psoriasis
Is the most common chronic inflammatory dermatome s affecting 1-2% of western world populations
Increased risk of heart attacks and stroke risks due to chronic inflammation
**psoriatic arthritis is seen in 10% of all psoriasis patients.
Pathogenesis of psoriasis
Is a T-cell mediated inflammatory disease which is believed to be autoimmune in origin but are not well described
- includes CD4/8 and T helper cells that accumulate in the epidermis
T-cells secrete cytokines and growth factors that induce keratinocytes hyperprolfieration which leads to characteristic lesions
There is both genetic and environmental reactors that contribute to the risk of psoriasis
- HLA loci and TNF signaling are the most likely genetic risks
Koebner phenomenon
Psoriatic lesions that are induced in susceptible individuals by local trauma
Auspitz sign
Seen in psoriasis
- when scraping the psoriatic patch, the lesion easily bleeds.
What are the most common locations for psoriasis?
Skin of elbows, knees, scalp, lumbosacral areas, penis and vulva.
Nails, fingers and toes = 30%
Treatment of psoriasis
Mild disease = corticosteroids
Severe = phototherapy, systemic therapies and methotrexate
Seborrheic dermatitis
Chronic inflammatory cause that affects 5% of the general population
Most common found in areas of high density of sebaceous glands
- scalp, forehead, external auditory canal and labia folds of the nose
Pathogenesis = unknown
- increased sebum production is believed to play a part but not definitive
- also possible relationship between malassezia fungal species but inconclusive
Lichen planus
Uncommon disorders that usually presents in middle-aged adults a
- produces multiple cutaneous lesions around extremities, vulva and penis on squamous mucosa. Pruritic, purple, planar papules and plaques
- *70% can show oral mucosa lichen planus
**Is CD8 Tcell mediated cytotoxic response within the basal cell layer. Cause is unknown but is believed to be viral or drug exposure response
Treatment = usually resolve spontaneously within 1-2 years.
How to tell lichen planus from erythema multiforme histologically
lichen planus shows well-developed changes in chronicity which includes epidermal hyperplasia, hypergranulosis and hyperkeratosis
Acne vulgaris
Virtually universal in the middle to late teenage years of everyone
- Asians tend to get in more mild
- is exacerbated by drugs, occupational exposures and heavy use of cosmetics or living in humid conditions
Can be inflammatory and non-inflammatory types (however a person can have both at the same time)
Non inflammatory types can show with open and closed comedones
- open comedones = small follicular papules containing central black keratin plugs
- closed comedones = follicular papules without a visible central plug
4 factors that contribute to acne vulgaris
1) keratinization of the lower portion of the hair follicle and development of a keratin plug
- blocks the outflow of sebum to the skin surface
2) hypertrophy of sebaceous glands during puberty due to increased levels of androgens
3) lipase-synthesizing bacteria colonizing the upper portions of the hair follicle which convert sebum lipids to pro inflammatory fatty acids
- especially P. Acnes
4) secondary inflammation of the involved follicle
What is the synthetic vitamin A derivative used in severe acne cases?
13-cis-retinoic acid (isotretinoin)
Rosacea
Common disease of middle age and beyond which affects 3% of the US population with preference towards females
4 stages of rosacea
1) flushing episodes
2) persistent erythema and telangiectasia
3) pustules and papules
4) rhinophyma
- permanent thickening of the nasal skin by confluent erythematous papules and prominent follicles
Pathogenesis of rosacea
Individuals present with high cutaneous levels of the antimicrobial peptide cathelicidin
- this peptide is a mediator of the cutaneous innate immune response
These peptides are qualitatively different from patents without rosacea. And injection of these peptides induces cutaneous changes seen in rosacea including inflammation and vascular dilation as well as increases in chemotaxis, angiogenesis and cytokine production
also increased activation of toll-like receptor 2 (TLR2) upregulates kallikrein 5 expression in keratinocytes.