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.
Impetigo
Superficial bacterial infection of the skin characterized by accumulation of neutrophils beneath the stratum corneum producing sub corneal pustule
- super common in children vs adults
Pretty much only caused by staphylococcus aureus and streptococcus pyogenes through direct contact with a source
- often begins as a small macula on the extremities or near the face/nose/mouth. Overtime evolves into larger lesions with “honey-colored” crust due to dried serum
Superficial fungal infections
Fungal infections that are confined to the stratum corneum and are primarily caused by dermatophytes
Tons of subsets but all begin with “tinea” and are based on locations
- tinea capitis = head (ringworm)
Asymptomatic with hairless patches of skin and crust forming
- tinea Barbae = beard
- Tinea corporis = trunk surface (mostly feet and nails)
Expanding, round, slightly erythematous plaque with elevated scaling border. Excessive heat and humidity increases chances - tinea cruris = inguinal areas of obese men due to increased heat and friction
- tinea pedis = athletes foot and infection of the toe nails
Affects 30-40% of population that shows erythema within webs of feet and toes. Also can spread to the nails (referred to onychomycosis) - tinea versicolor = upper trunk and is caused by malassezia furfur. Lesions consist of groups of macules with varied size and color with fine peripheral scales
Verrucae (warts)
Proliferative lesions of squamous epithelial cells
- caused by human papilloma virus (HPV)
- cutaneous warts are mainly caused by low-risk HPV types (1/2/3/4/10) (these lack transforming potential)
Most common in children but can be seen in any group
the more immunodeficient one is, the larger and more neurons the warts become (however there is no increased risk of cancer unless they become infected with high risk HPV subtypes
Generally self-limiting and regress spontaneously within 6 months- 2 yrs
Pathogenesis of verrucae
E6/E7 proteins in HPV viruses increase dysregulated epidermal cell growth and prevention of apoptosis
- this is seen in low and high risk HPV types
main difference in low-risk subtypes (why they dont cause cancer) is that structural variation fo these proteins limits their interactions with host proteins which limits the amount fo hyperplastic growth
Verruca vulgaris
Most common type of wart that can be found anywhere on the body
- shows grey white-tan conveys 0.1-1cm papules with rough pebble like surfaces
Verruca plantaris and palmaris
Warts that occur on the soles and palms respectively
- are rough scaly lesions that reach 1-2 cm in diameter and may coalesce to form a surface that looks similar to ordinary calluses
Condylomata acumunatum
Veneral warts
Occurs on the penis, urethra and perianal areas
Molluscum contagiosum
Common self-limiting viral disease of the skin that is caused by pox virus
Spread via direct contact is particularly common amoung children
Presents with multiple lesions that are pruritic, pink-tan umbilicated papules
- range in size from 0.2-0.4 cm
