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derm A 2 Flashcards

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Dermatology Board Prep flashcards
1
Q

pilosebaceous unit

A

-hair shaft
- Hair follicule
- sebaceous gland

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2
Q

Sebaceous glands

A
  • 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
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3
Q

holocrine process

A

-> entire cell breaks down to release contents (all of the cell breaks open to release sebum contents –> secretion from constantly dying cells)

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4
Q

pilosebaceous unit - acne

A

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)

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5
Q

pilosebaceous unit - hair growth cycle

A

ranges from few months to years depending on body site
- hair shaft = packed keratinocytes specialized
- length depends on body site

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6
Q

epidermis KC replication - normal

A

-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

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7
Q

interfollicular stem cells (between hair follicles)

A
  • 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

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8
Q

follicular stem cells (“bulge”) –> hair follicle

A
  • 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

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9
Q

epidermal KC replication diseases: benign - psoriasis

A
  • ~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)
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10
Q

epidermal KC replication diseases: benign - psoriasis HISTOLOGY

A
  • 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
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11
Q

epidermal KC replication diseases: possible precursors to keratinocyte malignancy. 1

A

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

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12
Q

epidermal KC replication diseases: possible precursors to keratinocyte malignancy. 2

A

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

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13
Q

epidermal KC replication diseases: AK and KA therapy

A
  • physical: surgery, dermabrasion, laser resurfacing
  • drug: topical cyto-toxic drug (short-term) –> target and stop mitosis of hyperplastic cells
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14
Q

epidermal KC replication diseases: skin malignancies - keratinocyte (non-melanoma)

A

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)

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15
Q

BCC & SCC: shared risk factors

A
  • 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
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16
Q

epidermal KC replication diseases: BCC PRESENTATION AND HISTOLOGY

A

basal cell carcinoma
- presentation: pearly nodule, central depression, rolled edge
- histology: look like immature or “basal” cells of epidermis, slow growing (rarely metastasize)

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17
Q

epidermal KC replication diseases: BCC etiology and treatment

A
  • 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)
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18
Q

epidermal KC replication diseases: SCC PRESENTATION AND HISTOLOGY

A

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

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19
Q

epidermal KC replication diseases: SCC etiology and treatment

A
  • 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)
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20
Q

malignant melanoma (ABCDEs) –> skin cancer derived from melanocytes

A
  • 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)

21
Q

ABCDE - good

A
  • symmetry, smooth border, light/med/dark brown, no bigger than a pencil eraser, slight dome or flat
22
Q

ABCDE - bad

A
  • 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
23
Q

dermis - organization & cell types

A
  • 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
24
Q

dermis: 2 histological compartments

A
  1. papillary dermis - undulating projections at the interface, more organized collagen, finer capillaries
  2. reticular dermis - the bulk of the dermis, extra extracellular matrix, thicker collagen fibrils
    - overall, similar
25
Q

dermis: papillary dermis

A

-Immediately under basal lamina
-fine mesh of collagen fibrils - small vessels & capillary beds supply the dermis AND epidermis and sensory nerve endings
- undulating arrangement - more contact area between epidermis & dermis per unit of surface provides stronger attachment

26
Q

dermis: reticular dermis

A
  • dense collagen fibrils - larger blood vessels and dilation/constriction promote / restrict heat loss
  • nerves, base of hair follicles & sweat glands
27
Q

1st degree (mild sunburn)

A
  • damage within epidermis
  • transient dermal erythema
  • heals 4-5 days; no scarring
  • redness = expansion of vasculature
  • only damage to a few KCs in the epidermis
28
Q

2nd degree (note depths - varying)

A
  • in dermis
  • blister fluid may separate epidermis from dermis
  • painful; nerve endings viable
  • heals in ~2 weeks
  • regrowth: KCs w/in follicles
  • always leaves a bit of hair follicle
29
Q

3rd degree (eschar)

A
  • follicles, glands destroyed dermis may be lost (base of hair follicle lost)
  • under lowest part of hair follicle –> lost reservoir of healing cells (bulge)
  • injury depth kills nerves; less pain than 2nd degree
  • wounds <5cm diameter heal from edge
  • wounds > or = ~5cm diameter require grafting (if diameter is too big, KCs cannot replicate and migrate to wider diameter)
30
Q

skin surface area: rule of nines - adults

A

9% of each of 11 sites
- all of head & neck
- R & L anterior trunk
- R & L posterior trunk
- R & L arm
- R & L anterior leg
- R & L posterior leg
- 1% - groin

31
Q

skin surface area: critical burns

A

burns critical if
- >25% of body has 2nd degree burns
- >10% of body has 3rd degree burns
- area affects amt of fluid loss & increases infection rate
- adverse drug reactions (ADR) –> estimating involved skin area w/ blistering, rash, etc. from medication reaction

32
Q

skin wound healing - stages

A

get HIP-R (often overlap) –> next stage usually begins before prior stage is complete
- hemostasis
- inflammation
- proliferation
- remodeling

33
Q

skin wound healing: hemostasis

A

minutes-hours
- vasoconstriction; platelet aggregation & blood clotting

34
Q

skin wound healing: inflammation

A

hrs-days/weeks (depending on the wound size)
- early acute phase: vasodilation & capillary permeability chemotaxis of leukocytes
- late acute (possibly chronic) phase: macrophages infiltration

35
Q

skin wound healing: proliferation

A

days-weeks
- KCs, fibroblasts, endothelial cells
- synthesis & deposition of matrix; excess matrix & fibroblasts lead to keloid (hypertrophic scar)

36
Q

skin wound healing: remodeling

A

weeks-years
- scar contraction: myofibroblast cells
- scar maturation: collagen cross-linking

37
Q

skin ADR - MP rash/SJS/TEN

A

skin-manifested ADR - a continuum of 3 individual pathologies?
- MP rash - maculo-papular rash
- SJS - steven johnson’s syndrome = skin erosion of keratinocytes
- TEN - toxic epidermal necrolysis = huge sheet of epidermis peels off
- use rule of 9s

38
Q

MP rash/SJS/TEN

A

3 names may be different extent of same pathology
- diagnosis dependent on physical, histological, biochemical criteria
- erythematous –> skin loss; severity associated with nomenclature
- MP does NOT necessarily progress to SJS/TEN; TEN is NOT necessarily preceded by MP

39
Q

drugs associated with MP/SJS/TEN

A

~100 different drugs associated with MP/SJS/TEN
- triggers degradation of the skin in predisposed populations
- minimum number of drugs associated w/ majority of cases
principals
- antibacterial sulfonamides & antibiotics (ex. penicillin-related)
- aromatic anticonvulsants (ex. phenobarbital)
- NSAIDs (ex. piroxicam

40
Q

SJS/TEN - tissue & cellular levels

A
  • histopathology: KC apoptosis & necrosis, blistering at dermal junction
  • apoptotic signals
  • reactive oxygen species (ROS) production secondary to electrophilic drug metabolites –-> cell membrane damage & necrosis
  • ROS stimulates production of NO (nitric oxide)
  • NO stimulates keratinocyte apoptosis
41
Q

SJS/TEN - mechanism
uncertain mechanism

A
  • ~50:1 medline hits for incidence vs. mechanism
  • genetic predisposition? (HLA, CYP SNPs)
  • other predisposing factors: subacute viral infection, low level auto-immune disease (stimulation of immune system already)
  • novel antigen of drug/protein combination
  • the “perfect storm” combo of factors (whole cluster of co-presenting events)
42
Q

primary therapy for SJS/TEN

A
  • identification & cessation of suspect drug –
  • problems: drug half-life, slow metabolizers, compromised excretion; symptoms can occur weeks after initial exposure
  • usually admitted to burn unit
  • monitor airways for involvement
43
Q

secondary therapy for SJS/TEN

A
  • plasmapheresis: patient’s blood cells + donor plasma reinfused into patient to remove nondialyzable drug, metabolite etc.
  • remove the patient’s serum and add donor serum (serum is the one causing ADR)
44
Q

therapy - severe cases: supportive care

A
  • pain management
  • hydration, occlusion to prevent drying
  • nutrition: hypercaloric & high-protein diet
  • cyclosporin & glucocorticoids to decrease inflammation BUT may decrease ability to fight infection
  • antibiotics controversial: aggravating adverse drug reaction?
45
Q

sweat glands: eccrine & apocrine

A

differ
- in distribution, association (or not) with hair follicle, innervation, stimulus, and type of sweat produced

46
Q

sweat glands: eccrine

A
  • distribution: across body surface
  • opening: skin surface
  • innervation: cholinergic nerves
  • stimulus: increases body temp
  • product: dilute electrolyte
47
Q

sweat glands: apocrine

A
  • distribution: axillary & perineal
  • opening: hair follicle
  • innervation: adrenergic nerves
  • stimulus: emotion or pain
  • product: electrolyte & lipid
48
Q

adnexal structures - nails

A
  • nail plate - on nail bed, specialized epidermal area –> extensive underlying vascular supply responsible for pink color of nails
  • matrix - mitotically active keratinocytes in nail bed –> produce the nail plate
  • lunula - thickened area in nail plate distal to cuticle –> high mechanical strength but low lipid & high water loss

derm (5 decks)

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