derm A 2 Flashcards
(48 cards)
pilosebaceous unit
-hair shaft
- Hair follicule
- sebaceous gland
Sebaceous glands
- throughout the epidermis EXCEPT THE PALSM AND SOLES
- face and scalp have hte highest denisty and size variation
- empties into upper hair folecule
- sebum production stimulated by androgens
- secretion via holocrine process
- replicating cells (mitotic) at gland perimeter replace those lost
- sebaceous gland cells have nuclei and clear lipid/sebum around
holocrine process
-> entire cell breaks down to release contents (all of the cell breaks open to release sebum contents –> secretion from constantly dying cells)
pilosebaceous unit - acne
sebocytes & KCs
- hypersecretion & hyperproliferation, respectively, blocks duct and/or hair follicle (keratinocytes lining hair follicle hyperproliferate, plugging follicle and increasing infection)
- accutane (13-cis retinoic acid) decrease KC proliferation and decreases sebum production (slows chance of plugging opening)
pilosebaceous unit - hair growth cycle
ranges from few months to years depending on body site
- hair shaft = packed keratinocytes specialized
- length depends on body site
epidermis KC replication - normal
-cells build physical strata & functional barrier
- physiological requirement to maintain a lifetime replacement of upper layers
- normal turnover
- wound healing
LOOK AT PICTURE SLIDE 14
interfollicular stem cells (between hair follicles)
- normal site of replication in basal layer only (basal layer stem cells replicate)
- responsible for routine replacement of epidermis & minor wounds (filling in the void)
LOOK AT PICTURE SLIDE 14
follicular stem cells (“bulge”) –> hair follicle
- important for healing of 2 degree burns (incredibly important for major wound healing)
- progeny contribute to epidermis and hair
- stem cell “bulge” gives rise to keratinocytes
- fibroblasts in dermal papilla “instruct” bulge daughter KCs to follow hair KC maturation –> instruct incoming KCs to change their gene patterns to make keratins specific to the hair shaft (push tip of hair out of the hair follicle)
- re-epithelialize –> recover what was stripped away from the epidermis surface
LOOK AT SLIDE 14
epidermal KC replication diseases: benign - psoriasis
- ~3% of US population –> genetic component?: first degree relative of patient more likely to develop symptoms
- presentation - varying severity
- symmetric, well-demarcated, plaques often on elbows, knees, scalp, & lower back
- plaques –> over-replication of keratinocytes in large areas
- reddened, inflamed, itch (characteristic of hyperplastic disease)
epidermal KC replication diseases: benign - psoriasis HISTOLOGY
- hyperproliferation (overaccumulation of keratinocytes)
- hyperkeratosis - increased but immature SC layers
- parakeratosis - nuclei retained in SC incomplete maturation (nuclei normally broken down from granular to cornified)
- SG may be reduced
- very poor barrier function; “more” isn’t better –> incompletely matured keratinocytes
- immune cell infiltration
- infection, fluid leakage
- missing stratum granulosum layer and thicker epidermis layer
- still basal separation between the dermis and epidermis
epidermal KC replication diseases: possible precursors to keratinocyte malignancy. 1
actinic keratoses (AK)
- chronic sun exposure
- chiefly on face, ears, & forearms (overexposure to the sun)
- individual or multiple sites, scaly, red
- ~20% develop malignancy over 10-25 years
- does not go away without treatment
epidermal KC replication diseases: possible precursors to keratinocyte malignancy. 2
keratoacanthoma (KA)
- usually solitary nodule often same areas as AK
- rapidly growing; 2.5cm in only 3-8 weeks
- frequently, spontaneously regress
- some later develop malignancy at same site
- THE TOMATO ON THE FACE
epidermal KC replication diseases: AK and KA therapy
- physical: surgery, dermabrasion, laser resurfacing
- drug: topical cyto-toxic drug (short-term) –> target and stop mitosis of hyperplastic cells
epidermal KC replication diseases: skin malignancies - keratinocyte (non-melanoma)
skin cancers
- ~3 million TOTAL cases diagnosed in US per year are unevenly distributed among types
- ~80% BCC - basal cell carcinoma vs. ~20% SCC - squamous cell carcinoma
- ~95% cure rate for both if detected & treated early
- commonly diagnosed but relatively high cure rate
- most occur in pts >60 yo –> “cancer”: a time-dependent accumulation of multiple mutations? (progressive series of mutations can lead to cancerous KC phenotype)
BCC & SCC: shared risk factors
- sun, indoor tanning, fair-skin (UV exposure)
- chemical exposure, ex. arsenic (contaminated drinking water)
- immunosuppression or compromised immune system (AIDS/organ transplant ~20-200x) –> may not remove tumor cells with altered antigens otherwise recognized as NON-self
epidermal KC replication diseases: BCC PRESENTATION AND HISTOLOGY
basal cell carcinoma
- presentation: pearly nodule, central depression, rolled edge
- histology: look like immature or “basal” cells of epidermis, slow growing (rarely metastasize)
epidermal KC replication diseases: BCC etiology and treatment
- etiology: UV exposure induces DNA mutations ex. in p53 tumor suppressor gene (normal p53 arrests cell cycle, allows time for DNA repair)
- treatment therapy: no single method ideal –> surgical excision (may be difficult to remove all of the islands), radiation, retinoids (vitamin A derivative) to suppress cell replication
- retinoic acid (acidic form of vitamin A)
epidermal KC replication diseases: SCC PRESENTATION AND HISTOLOGY
squamous cell carcinoma
- presentation: early stage vs. late stage
- early stage: indurated (hardened), erythematous plaque
- late stage: ulceration/crusting often indicating invasion of underlying tissue
- histology: cells look like squame KCs, irregular masses of proliferating KCs extend into dermis, “keratin pearls” in differentiated tumors
epidermal KC replication diseases: SCC etiology and treatment
- etiology: similar to BCC, UV exposure
- treatment/therapy: surgery, usually followed by radiation or chemotherapy (ex. retinoids to suppress replication of anything the surgery did not remove)
malignant melanoma (ABCDEs) –> skin cancer derived from melanocytes
- incidence: ~100,000 cases yr (~ 7,000) deaths /yr
- etiology/risk factors: fair skin & congenital nevi already present (moles), family history of melanoma, history of chronic sun exposure (UV)
- presentation: greatly variable in size, shape, color, atypical ABCDE (especially >5-6mm)
treatment/therapy:
- excision of lesion and nearby uninvolved skin and evaluation of lymph nodes for possible spread, often followed with interferon (suppress growth)
ABCDE - good
- symmetry, smooth border, light/med/dark brown, no bigger than a pencil eraser, slight dome or flat
ABCDE - bad
- no symmetry, change in pigmentation, raised
- some parts of the malignant melanoma might have no pigment because there were so many mutations that it lost its function to make melanin but is still growing
dermis - organization & cell types
- extracellular matrix (ECM) protein - mostly collagen, some laminin,multiple cell types
- fibroblasts produce collagen & other ECM proteins
- macrophages & mast cells peripheral immune function, some antigen processing (langerhans from blood vessels traveling to/from the epidermis)
- endothelial cells walls of blood vessels
- sensory nerve endings
dermis: 2 histological compartments
- papillary dermis - undulating projections at the interface, more organized collagen, finer capillaries
- reticular dermis - the bulk of the dermis, extra extracellular matrix, thicker collagen fibrils
- overall, similar
