Facial Plastic And Reconstructive Surgery

Front 1

koebner phenomenon

Back 1

predispostiion of certain cutaneous diseases to localize in areas of scars regardless of how carefully the surgery is performed.

Front 2

Endogenous changes of skin

Back 2

fine wrinkling, dermal atrophy, decrease in subdermal adipose tissue. Also loss of elastic fibers

Front 3

5 layers of epidermis

Back 3

1. basal - straum germinativum
2. Prickle - stratum spinosum
3. stratum granulosum
4. stratum corneum
5. stratum lucidum

Front 4

Langerhans cells

Back 4

features of monocytes and macrophages and are thought to migrate to skin from bone marrow. Clear cells

Prickle Cell layer

Front 5

Merkel Cells

Back 5

basal cell layer

associated with terminal nerves.

Light touch discrimination

Front 6

Dermis layers

Back 6

papillary dermis- thin
reticular dermis- thick

Front 7

telangiectatic vessels on face

Back 7

they are arteriole and red.
respond well to lasers in yellow portion of electromagnetic spectrum

repond poor to sclerosing agents.

telangiectatic vessels on legs are opposite.

Front 8

meissner corpuscles

Back 8

sensation of touch
dermal papillae
string wound around a spindle

Front 9

Vater-Pacini corpuscles

Back 9

sensation of pressure
superficial fascia
oval bodies with concentric lamellae

Front 10

meibomian glands

Back 10

sebaceous glands on eyelids
Cause of chazalion

Front 11

eccrine glands

Back 11

sweat glands

Front 12

meissner corpuscles

Back 12

sensation of touch
dermal papillae
string wound around a spindle

Front 13

Vater-Pacini corpuscles

Back 13

sensation of pressure
superficial fascia
oval bodies with concentric lamellae

Front 14

Chalazion

Back 14

Chalazion, meaning "hail stone" in Greek, is a chronic inflammatory lesion that develops when a Zeis or meibomian tear gland of the eyelid becomes obstructed. A chalazion may first present with eyelid swelling and erythema and then evolve into a painless, rubbery, nodular lesion. It is seen commonly in patients with eyelid margin blepharitis and in those with rosacea. An inflamed hordeolum will often calm and scar into a hard chalazion (see 'Hordeolum' below).

Treatment — Antibiotics are not indicated since chalazion is a granulomatous condition. Small chalazia often resolve without intervention. For larger lesions, frequent hot compresses may allow them to drain although typically most clear spontaneously in weeks to months. Symptomatic patients with recalcitrant lesions can be referred to an ophthalmologist for incision and curettage or direct glucocorticoid injection

Front 15

meibomian glands

Back 15

sebaceous glands on eyelids
Cause of chazalion

Front 16

eccrine glands

Back 16

sweat glands

Front 17

Chalazion

Back 17

Chalazion, meaning "hail stone" in Greek, is a chronic inflammatory lesion that develops when a Zeis or meibomian tear gland of the eyelid becomes obstructed. A chalazion may first present with eyelid swelling and erythema and then evolve into a painless, rubbery, nodular lesion. It is seen commonly in patients with eyelid margin blepharitis and in those with rosacea. An inflamed hordeolum will often calm and scar into a hard chalazion (see 'Hordeolum' below).

Treatment — Antibiotics are not indicated since chalazion is a granulomatous condition. Small chalazia often resolve without intervention. For larger lesions, frequent hot compresses may allow them to drain although typically most clear spontaneously in weeks to months. Symptomatic patients with recalcitrant lesions can be referred to an ophthalmologist for incision and curettage or direct glucocorticoid injection

Front 18

xanthelasma

Back 18

Xanthelasma are cholesterol-filled, soft, yellow plaques that usually appear on the medial aspects of the eyelids bilaterally. They most often occur in middle-aged and older adults.

Hyperlipidemia is present in approximately 50 percent of patients with xanthelasma. These lesions are a classic feature of primary biliary cirrhosis, a condition often associated with marked hypercholesterolemia. They are also common in patients with primary disorders of low-density-lipoprotein (LDL)-cholesterol metabolism; they occur in 75 percent of older patients with familial hypercholesterolemia, and 10 percent of patients with hyperapobetalipoproteinemia. Young individuals, in particular, with xanthelasma, appear to have a relatively high prevalence of lipoprotein abnormalities.

In normolipidemic individuals, the possible association between xanthelasma and atherosclerosis is not clear. Some studies have noted other lipoprotein abnormalities in normocholesterolemic patients with xanthelasma that may increase the risk of coronary heart disease, including low levels of high-density-lipoprotein (HDL)-cholesterol. Thus, it is reasonable to obtain a lipid profile in patients with xanthelasma.

Treatment — Xanthelasma are always benign lesions. Therapy is usually undertaken only for cosmetic reasons.

Lipid lowering may induce regression of xanthelasma in some patients, although the effect is not consistent. Removal can be attempted with surgery, carbon dioxide laser, or topical 100 percent trichloroacetic acid (TCA), but recurrence is common.

Front 19

molluscum contagiosum

Back 19

Molluscum contagiosum is caused by a poxvirus and spread by direct contact or by fomites. It is usually seen as one or multiple small, pale, shiny nodules with central umbilication. A chronic conjunctivitis may accompany the condition if it is located on the lid margin. The diagnosis is based on clinical appearance; biopsy is rarely necessary.

Most patients with molluscum contagiosum are not immunodeficient, although approximately 10 to 20 percent of HIV-infected patients develop this infection on the face, neck, or anogenital areas. There may be more dissemination with confluent lesions in patients with immune deficiency states; these individuals can have up to 40 lesions on each eyelid.

Treatment — Molluscum may resolve spontaneously within one year. Treatment options include simple excision, cryotherapy, and desiccation.

Front 20

Apocrine glands

Back 20

odorless, but with bacteria = smells.
Most numerous axilla and groin.

Molls glands of eyelids
ceruminous glands of EAC

Front 21

sebaceious glands in wounds

Back 21

principal source of eptithelial regeneration in dermal injuries.

Front 22

Inflammatory Phase

Back 22

vasodilation 0-day 3
cellular response 30min-1wk

Front 23

Proliferative phase

Back 23

re-epithelialization few hrs - 1wk
Collagen synthesis - Day 2- 1mo
Wound contraction - day 5- 1mo

Front 24

Maturation/remodeling

Back 24

scar
collagen remodeling 2.5 wks - one year.

Front 25

Werner syndrome

Back 25

Adult progeria, premature aging
chromosome 8
poor wound healing
tx with vit c

Front 26

Wound Healing: Desiccation

Back 26

eptithelial cells migrate faster if there is adequate surface moisture
scabbed wounds heal much slower and require more energy
occlusive dressing allow healing more directly and efficiently.
semiocclusive and occlusive dressing heal the same b/c minimal O2 is absorbed through wound. Dressing increases healing by 50%.

Neosporin and silvadene increased healing by 28%.

Front 27

Wound Healing: Ischemia

Back 27

O2 consumption is higher in a healing wound
tissue injury results in reduced oxygen.
fibroblast and collagen synthesis to occur a pO2 of 30-40mm Hg is necessary.

Front 28

Wound healing: insulin

Back 28

microangiopathy diminishes O2 delivery.
insulin deficiency significant in early wound healing when leukocyte fxn is defective.
Increases chance for infection.

Low insulin leads to defective collagen synthesis.

Front 29

Hypertrophic scar vs Keloids

Back 29

hypertrophic scars - elevated and remain within the original tissue injury site, tend to regress.
Keloids: overgrow the boundaries of original injury and invade the surrounding normal tissue.

Front 30

Scar and Keloid tx

Back 30

directed at inhibiting collagen overproduction by a combo of intralesional corticosteriods and occasionally excision with post-op pressure dressings, silicon gel sheeting, interferon-a2b.

Front 31

Fusiform Excision

Back 31

must always be designed in an RSTL and with a length-to-width ratio of 2.5:1 to 3:1, thus helping to avoid the standing cone or dog-ear deformity at the ends of the wound on closure

Front 32

Resting Skin Tension Lines

Back 32

they will always be perpendicular to the orientation of muscle fibers. The only exception is around the eye where the RSTLs parallel the musculus orbicularis oculi fibers

Front 33

Dog Ear, Standing cone deformity

Back 33

dog-ear or standing cone deformity results from the rotation of skin around a pivot point. The excess skin and advancement collects in the shape of a cone. The formation of these dog ears can be predicted and pre- vented by the excision of excess tissue that permits the stand- ing cone to lay flat. Burow’s triangle is a simple example of this execution and should ideally be designed to parallel the excision lines in the RSTLs for best camouflage. To flatten a standing cone, an inferiorly based triangle is excised, akin to the door flap of a tee-pee.

Front 34

Excising a lesion

Back 34

instead of creat- ing the cut at right angles to the skin surface, bevel the inci- sion outward (Fig. 3–9). This accomplishes the following: it aids in skin edge eversion, which is helpful in preventing depressed scars; it helps to create the plane for undermining; and it gives better assurance of completely excising around the lesion.

Front 35

Undermining

Back 35

The facial nerve branches pass deep to all of the mimetic musculature except those branches that emerge superficially to innervate the lateral fibers of the orbicularis oris, approximately 1 to 2 cm from the lateral commissure. Undermining should be used in virtually all surgical proce- dures in the skin of the head and neck and should be done completely around the incision, the ends as well as the sides, for a distance of about 2 cm from the wound edges.